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1. Rhythmic IL-17 production by γδ T cells maintains adipose de novo lipogenesis

Author

Douglas, Aaron, Stevens, Brenneth, Rendas, Miguel, Kane, Harry, Lynch, Evan, Kunkemoeller, Britta, Wessendorf-Rodriguez, Karl, Day, Emily A., Sutton, Caroline, Brennan, Martin, O’Brien, Katie, Kohlgruber, Ayano C., Prendeville, Hannah, Garza, Amanda E., O’Neill, Luke A. J., Mills, Kingston H. G., Metallo, Christian M., Veiga-Fernandes, Henrique, and Lynch, Lydia

Published
2024
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2. Effects of empagliflozin on progression of chronic kidney disease: a prespecified secondary analysis from the empa-kidney trial

Author

Staplin, N, Haynes, R, Judge, PK, Wanner, C, Green, JB, Emberson, J, Preiss, D, Mayne, KJ, Ng, SYA, Sammons, E, Zhu, D, Hill, M, Stevens, W, Wallendszus, K, Brenner, S, Cheung, AK, Liu, ZH, Li, J, Hooi, LS, Liu, WJ, Kadowaki, T, Nangaku, M, Levin, A, Cherney, D, Maggioni, AP, Pontremoli, R, Deo, R, Goto, S, Rossello, X, Tuttle, KR, Steubl, D, Petrini, M, Seidi, S, Landray, MJ, Baigent, C, Herrington, WG, Abat, S, Abd Rahman, R, Abdul Cader, R, Abdul Hafidz, MI, Abdul Wahab, MZ, Abdullah, NK, Abdul-Samad, T, Abe, M, Abraham, N, Acheampong, S, Achiri, P, Acosta, JA, Adeleke, A, Adell, V, Adewuyi-Dalton, R, Adnan, N, Africano, A, Agharazii, M, Aguilar, F, Aguilera, A, Ahmad, M, Ahmad, MK, Ahmad, NA, Ahmad, NH, Ahmad, NI, Ahmad Miswan, N, Ahmad Rosdi, H, Ahmed, I, Ahmed, S, Aiello, J, Aitken, A, AitSadi, R, Aker, S, Akimoto, S, Akinfolarin, A, Akram, S, Alberici, F, Albert, C, Aldrich, L, Alegata, M, Alexander, L, Alfaress, S, Alhadj Ali, M, Ali, A, Alicic, R, Aliu, A, Almaraz, R, Almasarwah, R, Almeida, J, Aloisi, A, Al-Rabadi, L, Alscher, D, Alvarez, P, Al-Zeer, B, Amat, M, Ambrose, C, Ammar, H, An, Y, Andriaccio, L, Ansu, K, Apostolidi, A, Arai, N, Araki, H, Araki, S, Arbi, A, Arechiga, O, Armstrong, S, Arnold, T, Aronoff, S, Arriaga, W, Arroyo, J, Arteaga, D, Asahara, S, Asai, A, Asai, N, Asano, S, Asawa, M, Asmee, MF, Aucella, F, Augustin, M, Avery, A, Awad, A, Awang, IY, Awazawa, M, Axler, A, Ayub, W, Azhari, Z, Baccaro, R, Badin, C, Bagwell, B, Bahlmann-Kroll, E, Bahtar, AZ, Bains, D, Bajaj, H, Baker, R, Baldini, E, Banas, B, Banerjee, D, Banno, S, Bansal, S, Barberi, S, Barnes, S, Barnini, C, Barot, C, Barrett, K, Barrios, R, Bartolomei Mecatti, B, Barton, I, Barton, J, Basily, W, Bavanandan, S, Baxter, A, Becker, L, Beddhu, S, Beige, J, Beigh, S, Bell, S, Benck, U, Beneat, A, Bennett, A, Bennett, D, Benyon, S, Berdeprado, J, Bergler, T, Bergner, A, Berry, M, Bevilacqua, M, Bhairoo, J, Bhandari, S, Bhandary, N, Bhatt, A, Bhattarai, M, Bhavsar, M, Bian, W, Bianchini, F, Bianco, S, Bilous, R, Bilton, J, Bilucaglia, D, Bird, C, Birudaraju, D, Biscoveanu, M, Blake, C, Bleakley, N, Bocchicchia, K, Bodine, S, Bodington, R, Boedecker, S, Bolduc, M, Bolton, S, Bond, C, Boreky, F, Boren, K, Bouchi, R, Bough, L, Bovan, D, Bowler, C, Bowman, L, Brar, N, Braun, C, Breach, A, Breitenfeldt, M, Brettschneider, B, Brewer, A, Brewer, G, Brindle, V, Brioni, E, Brown, C, Brown, H, Brown, L, Brown, R, Brown, S, Browne, D, Bruce, K, Brueckmann, M, Brunskill, N, Bryant, M, Brzoska, M, Bu, Y, Buckman, C, Budoff, M, Bullen, M, Burke, A, Burnette, S, Burston, C, Busch, M, Bushnell, J, Butler, S, Büttner, C, Byrne, C, Caamano, A, Cadorna, J, Cafiero, C, Cagle, M, Cai, J, Calabrese, K, Calvi, C, Camilleri, B, Camp, S, Campbell, D, Campbell, R, Cao, H, Capelli, I, Caple, M, Caplin, B, Cardone, A, Carle, J, Carnall, V, Caroppo, M, Carr, S, Carraro, G, Carson, M, Casares, P, Castillo, C, Castro, C, Caudill, B, Cejka, V, Ceseri, M, Cham, L, Chamberlain, A, Chambers, J, Chan, CBT, Chan, JYM, Chan, YC, Chang, E, Chant, T, Chavagnon, T, Chellamuthu, P, Chen, F, Chen, J, Chen, P, Chen, TM, Chen, Y, Cheng, C, Cheng, H, Cheng, MC, Ching, CH, Chitalia, N, Choksi, R, Chukwu, C, Chung, K, Cianciolo, G, Cipressa, L, Clark, S, Clarke, H, Clarke, R, Clarke, S, Cleveland, B, Cole, E, Coles, H, Condurache, L, Connor, A, Convery, K, Cooper, A, Cooper, N, Cooper, Z, Cooperman, L, Cosgrove, L, Coutts, P, Cowley, A, Craik, R, Cui, G, Cummins, T, Dahl, N, Dai, H, Dajani, L, D'Amelio, A, Damian, E, Damianik, K, Danel, L, Daniels, C, Daniels, T, Darbeau, S, Darius, H, Dasgupta, T, Davies, J, Davies, L, Davis, A, Davis, J, Davis, L, Dayanandan, R, Dayi, S, Dayrell, R, De Nicola, L, Debnath, S, Deeb, W, Degenhardt, S, DeGoursey, K, Delaney, M, DeRaad, R, Derebail, V, Dev, D, Devaux, M, Dhall, P, Dhillon, G, Dienes, J, Dobre, M, Doctolero, E, Dodds, V, Domingo, D, Donaldson, D, Donaldson, P, Donhauser, C, Donley, V, Dorestin, S, Dorey, S, Doulton, T, Draganova, D, Draxlbauer, K, Driver, F, Du, H, Dube, F, Duck, T, Dugal, T, Dugas, J, Dukka, H, Dumann, H, Durham, W, Dursch, M, Dykas, R, Easow, R, Eckrich, E, Eden, G, Edmerson, E, Edwards, H, Ee, LW, Eguchi, J, Ehrl, Y, Eichstadt, K, Eid, W, Eilerman, B, Ejima, Y, Eldon, H, Ellam, T, Elliott, L, Ellison, R, Epp, R, Er, A, Espino-Obrero, M, Estcourt, S, Estienne, L, Evans, G, Evans, J, Evans, S, Fabbri, G, Fajardo-Moser, M, Falcone, C, Fani, F, Faria-Shayler, P, Farnia, F, Farrugia, D, Fechter, M, Fellowes, D, Feng, F, Fernandez, J, Ferraro, P, Field, A, Fikry, S, Finch, J, Finn, H, Fioretto, P, Fish, R, Fleischer, A, Fleming-Brown, D, Fletcher, L, Flora, R, Foellinger, C, Foligno, N, Forest, S, Forghani, Z, Forsyth, K, Fottrell-Gould, D, Fox, P, Frankel, A, Fraser, D, Frazier, R, Frederick, K, Freking, N, French, H, Froment, A, Fuchs, B, Fuessl, L, Fujii, H, Fujimoto, A, Fujita, A, Fujita, K, Fujita, Y, Fukagawa, M, Fukao, Y, Fukasawa, A, Fuller, T, Funayama, T, Fung, E, Furukawa, M, Furukawa, Y, Furusho, M, Gabel, S, Gaidu, J, Gaiser, S, Gallo, K, Galloway, C, Gambaro, G, Gan, CC, Gangemi, C, Gao, M, Garcia, K, Garcia, M, Garofalo, C, Garrity, M, Garza, A, Gasko, S, Gavrila, M, Gebeyehu, B, Geddes, A, Gentile, G, George, A, George, J, Gesualdo, L, Ghalli, F, Ghanem, A, Ghate, T, Ghavampour, S, Ghazi, A, Gherman, A, Giebeln-Hudnell, U, Gill, B, Gillham, S, Girakossyan, I, Girndt, M, Giuffrida, A, Glenwright, M, Glider, T, Gloria, R, Glowski, D, Goh, BL, Goh, CB, Gohda, T, Goldenberg, R, Goldfaden, R, Goldsmith, C, Golson, B, Gonce, V, Gong, Q, Goodenough, B, Goodwin, N, Goonasekera, M, Gordon, A, Gordon, J, Gore, A, Goto, H, Gowen, D, Grace, A, Graham, J, Grandaliano, G, Gray, M, Greene, T, Greenwood, G, Grewal, B, Grifa, R, Griffin, D, Griffin, S, Grimmer, P, Grobovaite, E, Grotjahn, S, Guerini, A, Guest, C, Gunda, S, Guo, B, Guo, Q, Haack, S, Haase, M, Haaser, K, Habuki, K, Hadley, A, Hagan, S, Hagge, S, Haller, H, Ham, S, Hamal, S, Hamamoto, Y, Hamano, N, Hamm, M, Hanburry, A, Haneda, M, Hanf, C, Hanif, W, Hansen, J, Hanson, L, Hantel, S, Haraguchi, T, Harding, E, Harding, T, Hardy, C, Hartner, C, Harun, Z, Harvill, L, Hasan, A, Hase, H, Hasegawa, F, Hasegawa, T, Hashimoto, A, Hashimoto, C, Hashimoto, M, Hashimoto, S, Haskett, S, Hauske, SJ, Hawfield, A, Hayami, T, Hayashi, M, Hayashi, S, Hazara, A, Healy, C, Hecktman, J, Heine, G, Henderson, H, Henschel, R, Hepditch, A, Herfurth, K, Hernandez, G, Hernandez Pena, A, Hernandez-Cassis, C, Herzog, C, Hewins, S, Hewitt, D, Hichkad, L, Higashi, S, Higuchi, C, Hill, C, Hill, L, Himeno, T, Hing, A, Hirakawa, Y, Hirata, K, Hirota, Y, Hisatake, T, Hitchcock, S, Hodakowski, A, Hodge, W, Hogan, R, Hohenstatt, U, Hohenstein, B, Hooi, L, Hope, S, Hopley, M, Horikawa, S, Hosein, D, Hosooka, T, Hou, L, Hou, W, Howie, L, Howson, A, Hozak, M, Htet, Z, Hu, X, Hu, Y, Huang, J, Huda, N, Hudig, L, Hudson, A, Hugo, C, Hull, R, Hume, L, Hundei, W, Hunt, N, Hunter, A, Hurley, S, Hurst, A, Hutchinson, C, Hyo, T, Ibrahim, FH, Ibrahim, S, Ihana, N, Ikeda, T, Imai, A, Imamine, R, Inamori, A, Inazawa, H, Ingell, J, Inomata, K, Inukai, Y, Ioka, M, Irtiza-Ali, A, Isakova, T, Isari, W, Iselt, M, Ishiguro, A, Ishihara, K, Ishikawa, T, Ishimoto, T, Ishizuka, K, Ismail, R, Itano, S, Ito, H, Ito, K, Ito, M, Ito, Y, Iwagaitsu, S, Iwaita, Y, Iwakura, T, Iwamoto, M, Iwasa, M, Iwasaki, H, Iwasaki, S, Izumi, K, Izumi, T, Jaafar, SM, Jackson, C, Jackson, Y, Jafari, G, Jahangiriesmaili, M, Jain, N, Jansson, K, Jasim, H, Jeffers, L, Jenkins, A, Jesky, M, Jesus-Silva, J, Jeyarajah, D, Jiang, Y, Jiao, X, Jimenez, G, Jin, B, Jin, Q, Jochims, J, Johns, B, Johnson, C, Johnson, T, Jolly, S, Jones, L, Jones, S, Jones, T, Jones, V, Joseph, M, Joshi, S, Judge, P, Junejo, N, Junus, S, Kachele, M, Kadoya, H, Kaga, H, Kai, H, Kajio, H, Kaluza-Schilling, W, Kamaruzaman, L, Kamarzarian, A, Kamimura, Y, Kamiya, H, Kamundi, C, Kan, T, Kanaguchi, Y, Kanazawa, A, Kanda, E, Kanegae, S, Kaneko, K, Kang, HY, Kano, T, Karim, M, Karounos, D, Karsan, W, Kasagi, R, Kashihara, N, Katagiri, H, Katanosaka, A, Katayama, A, Katayama, M, Katiman, E, Kato, K, Kato, M, Kato, N, Kato, S, Kato, T, Kato, Y, Katsuda, Y, Katsuno, T, Kaufeld, J, Kavak, Y, Kawai, I, Kawai, M, Kawase, A, Kawashima, S, Kazory, A, Kearney, J, Keith, B, Kellett, J, Kelley, S, Kershaw, M, Ketteler, M, Khai, Q, Khairullah, Q, Khandwala, H, Khoo, KKL, Khwaja, A, Kidokoro, K, Kielstein, J, Kihara, M, Kimber, C, Kimura, S, Kinashi, H, Kingston, H, Kinomura, M, Kinsella-Perks, E, Kitagawa, M, Kitajima, M, Kitamura, S, Kiyosue, A, Kiyota, M, Klauser, F, Klausmann, G, Kmietschak, W, Knapp, K, Knight, C, Knoppe, A, Knott, C, Kobayashi, M, Kobayashi, R, Kobayashi, T, Koch, M, Kodama, S, Kodani, N, Kogure, E, Koizumi, M, Kojima, H, Kojo, T, Kolhe, N, Komaba, H, Komiya, T, Komori, H, Kon, SP, Kondo, M, Kong, W, Konishi, M, Kono, K, Koshino, M, Kosugi, T, Kothapalli, B, Kozlowski, T, Kraemer, B, Kraemer-Guth, A, Krappe, J, Kraus, D, Kriatselis, C, Krieger, C, Krish, P, Kruger, B, Ku Md Razi, KR, Kuan, Y, Kubota, S, Kuhn, S, Kumar, P, Kume, S, Kummer, I, Kumuji, R, Küpper, A, Kuramae, T, Kurian, L, Kuribayashi, C, Kurien, R, Kuroda, E, Kurose, T, Kutschat, A, Kuwabara, N, Kuwata, H, La Manna, G, Lacey, M, Lafferty, K, LaFleur, P, Lai, V, Laity, E, Lambert, A, Langlois, M, Latif, F, Latore, E, Laundy, E, Laurienti, D, Lawson, A, Lay, M, Leal, I, Lee, AK, Lee, J, Lee, KQ, Lee, R, Lee, SA, Lee, YY, Lee-Barkey, Y, Leonard, N, Leoncini, G, Leong, CM, Lerario, S, Leslie, A, Lewington, A, Li, N, Li, X, Li, Y, Liberti, L, Liberti, ME, Liew, A, Liew, YF, Lilavivat, U, Lim, SK, Lim, YS, Limon, E, Lin, H, Lioudaki, E, Liu, H, Liu, J, Liu, L, Liu, Q, Liu, X, Liu, Z, Loader, D, Lochhead, H, Loh, CL, Lorimer, A, Loudermilk, L, Loutan, J, Low, CK, Low, CL, Low, YM, Lozon, Z, Lu, Y, Lucci, D, Ludwig, U, Luker, N, Lund, D, Lustig, R, Lyle, S, Macdonald, C, MacDougall, I, Machicado, R, MacLean, D, Macleod, P, Madera, A, Madore, F, Maeda, K, Maegawa, H, Maeno, S, Mafham, M, Magee, J, Mah, DY, Mahabadi, V, Maiguma, M, Makita, Y, Makos, G, Manco, L, Mangiacapra, R, Manley, J, Mann, P, Mano, S, Marcotte, G, Maris, J, Mark, P, Markau, S, Markovic, M, Marshall, C, Martin, M, Martinez, C, Martinez, S, Martins, G, Maruyama, K, Maruyama, S, Marx, K, Maselli, A, Masengu, A, Maskill, A, Masumoto, S, Masutani, K, Matsumoto, M, Matsunaga, T, Matsuoka, N, Matsushita, M, Matthews, M, Matthias, S, Matvienko, E, Maurer, M, Maxwell, P, Mazlan, N, Mazlan, SA, Mbuyisa, A, McCafferty, K, McCarroll, F, McCarthy, T, McClary-Wright, C, McCray, K, McDermott, P, McDonald, C, McDougall, R, McHaffie, E, McIntosh, K, McKinley, T, McLaughlin, S, McLean, N, McNeil, L, Measor, A, Meek, J, Mehta, A, Mehta, R, Melandri, M, Mené, P, Meng, T, Menne, J, Merritt, K, Merscher, S, Meshykhi, C, Messa, P, Messinger, L, Miftari, N, Miller, R, Miller, Y, Miller-Hodges, E, Minatoguchi, M, Miners, M, Minutolo, R, Mita, T, Miura, Y, Miyaji, M, Miyamoto, S, Miyatsuka, T, Miyazaki, M, Miyazawa, I, Mizumachi, R, Mizuno, M, Moffat, S, Mohamad Nor, FS, Mohamad Zaini, SN, Mohamed Affandi, FA, Mohandas, C, Mohd, R, Mohd Fauzi, NA, Mohd Sharif, NH, Mohd Yusoff, Y, Moist, L, Moncada, A, Montasser, M, Moon, A, Moran, C, Morgan, N, Moriarty, J, Morig, G, Morinaga, H, Morino, K, Morisaki, T, Morishita, Y, Morlok, S, Morris, A, Morris, F, Mostafa, S, Mostefai, Y, Motegi, M, Motherwell, N, Motta, D, Mottl, A, Moys, R, Mozaffari, S, Muir, J, Mulhern, J, Mulligan, S, Munakata, Y, Murakami, C, Murakoshi, M, Murawska, A, Murphy, K, Murphy, L, Murray, S, Murtagh, H, Musa, MA, Mushahar, L, Mustafa, R, Mustafar, R, Muto, M, Nadar, E, Nagano, R, Nagasawa, T, Nagashima, E, Nagasu, H, Nagelberg, S, Nair, H, Nakagawa, Y, Nakahara, M, Nakamura, J, Nakamura, R, Nakamura, T, Nakaoka, M, Nakashima, E, Nakata, J, Nakata, M, Nakatani, S, Nakatsuka, A, Nakayama, Y, Nakhoul, G, Naverrete, G, Navivala, A, Nazeer, I, Negrea, L, Nethaji, C, Newman, E, Ng, TJ, Ngu, LLS, Nimbkar, T, Nishi, H, Nishi, M, Nishi, S, Nishida, Y, Nishiyama, A, Niu, J, Niu, P, Nobili, G, Nohara, N, Nojima, I, Nolan, J, Nosseir, H, Nozawa, M, Nunn, M, Nunokawa, S, Oda, M, Oe, M, Oe, Y, Ogane, K, Ogawa, W, Ogihara, T, Oguchi, G, Ohsugi, M, Oishi, K, Okada, Y, Okajyo, J, Okamoto, S, Okamura, K, Olufuwa, O, Oluyombo, R, Omata, A, Omori, Y, Ong, LM, Ong, YC, Onyema, J, Oomatia, A, Oommen, A, Oremus, R, Orimo, Y, Ortalda, V, Osaki, Y, Osawa, Y, Osmond Foster, J, O'Sullivan, A, Otani, T, Othman, N, Otomo, S, O'Toole, J, Owen, L, Ozawa, T, Padiyar, A, Page, N, Pajak, S, Paliege, A, Pandey, A, Pandey, R, Pariani, H, Park, J, Parrigon, M, Passauer, J, Patecki, M, Patel, M, Patel, R, Patel, T, Patel, Z, Paul, R, Paulsen, L, Pavone, L, Peixoto, A, Peji, J, Peng, BC, Peng, K, Pennino, L, Pereira, E, Perez, E, Pergola, P, Pesce, F, Pessolano, G, Petchey, W, Petr, EJ, Pfab, T, Phelan, P, Phillips, R, Phillips, T, Phipps, M, Piccinni, G, Pickett, T, Pickworth, S, Piemontese, M, Pinto, D, Piper, J, Plummer-Morgan, J, Poehler, D, Polese, L, Poma, V, Postal, A, Pötz, C, Power, A, Pradhan, N, Pradhan, R, Preiss, E, Preston, K, Prib, N, Price, L, Provenzano, C, Pugay, C, Pulido, R, Putz, F, Qiao, Y, Quartagno, R, Quashie-Akponeware, M, Rabara, R, Rabasa-Lhoret, R, Radhakrishnan, D, Radley, M, Raff, R, Raguwaran, S, Rahbari-Oskoui, F, Rahman, M, Rahmat, K, Ramadoss, S, Ramanaidu, S, Ramasamy, S, Ramli, R, Ramli, S, Ramsey, T, Rankin, A, Rashidi, A, Raymond, L, Razali, WAFA, Read, K, Reiner, H, Reisler, A, Reith, C, Renner, J, Rettenmaier, B, Richmond, L, Rijos, D, Rivera, R, Rivers, V, Robinson, H, Rocco, M, Rodriguez-Bachiller, I, Rodriquez, R, Roesch, C, Roesch, J, Rogers, J, Rohnstock, M, Rolfsmeier, S, Roman, M, Romo, A, Rosati, A, Rosenberg, S, Ross, T, Roura, M, Roussel, M, Rovner, S, Roy, S, Rucker, S, Rump, L, Ruocco, M, Ruse, S, Russo, F, Russo, M, Ryder, M, Sabarai, A, Saccà, C, Sachson, R, Sadler, E, Safiee, NS, Sahani, M, Saillant, A, Saini, J, Saito, C, Saito, S, Sakaguchi, K, Sakai, M, Salim, H, Salviani, C, Sampson, A, Samson, F, Sandercock, P, Sanguila, S, Santorelli, G, Santoro, D, Sarabu, N, Saram, T, Sardell, R, Sasajima, H, Sasaki, T, Satko, S, Sato, A, Sato, D, Sato, H, Sato, J, Sato, T, Sato, Y, Satoh, M, Sawada, K, Schanz, M, Scheidemantel, F, Schemmelmann, M, Schettler, E, Schettler, V, Schlieper, GR, Schmidt, C, Schmidt, G, Schmidt, U, Schmidt-Gurtler, H, Schmude, M, Schneider, A, Schneider, I, Schneider-Danwitz, C, Schomig, M, Schramm, T, Schreiber, A, Schricker, S, Schroppel, B, Schulte-Kemna, L, Schulz, E, Schumacher, B, Schuster, A, Schwab, A, Scolari, F, Scott, A, Seeger, W, Segal, M, Seifert, L, Seifert, M, Sekiya, M, Sellars, R, Seman, MR, Shah, S, Shainberg, L, Shanmuganathan, M, Shao, F, Sharma, K, Sharpe, C, Sheikh-Ali, M, Sheldon, J, Shenton, C, Shepherd, A, Shepperd, M, Sheridan, R, Sheriff, Z, Shibata, Y, Shigehara, T, Shikata, K, Shimamura, K, Shimano, H, Shimizu, Y, Shimoda, H, Shin, K, Shivashankar, G, Shojima, N, Silva, R, Sim, CSB, Simmons, K, Sinha, S, Sitter, T, Sivanandam, S, Skipper, M, Sloan, K, Sloan, L, Smith, R, Smyth, J, Sobande, T, Sobata, M, Somalanka, S, Song, X, Sonntag, F, Sood, B, Sor, SY, Soufer, J, Sparks, H, Spatoliatore, G, Spinola, T, Squyres, S, Srivastava, A, Stanfield, J, Staylor, K, Steele, A, Steen, O, Steffl, D, Stegbauer, J, Stellbrink, C, Stellbrink, E, Stevenson, A, Stewart-Ray, V, Stickley, J, Stoffler, D, Stratmann, B, Streitenberger, S, Strutz, F, Stubbs, J, Stumpf, J, Suazo, N, Suchinda, P, Suckling, R, Sudin, A, Sugamori, K, Sugawara, H, Sugawara, K, Sugimoto, D, Sugiyama, H, Sugiyama, T, Sullivan, M, Sumi, M, Suresh, N, Sutton, D, Suzuki, H, Suzuki, R, Suzuki, Y, Swanson, E, Swift, P, Syed, S, Szerlip, H, Taal, M, Taddeo, M, Tailor, C, Tajima, K, Takagi, M, Takahashi, K, Takahashi, M, Takahashi, T, Takahira, E, Takai, T, Takaoka, M, Takeoka, J, Takesada, A, Takezawa, M, Talbot, M, Taliercio, J, Talsania, T, Tamori, Y, Tamura, R, Tamura, Y, Tan, CHH, Tan, EZZ, Tanabe, A, Tanabe, K, Tanaka, A, Tanaka, N, Tang, S, Tang, Z, Tanigaki, K, Tarlac, M, Tatsuzawa, A, Tay, JF, Tay, LL, Taylor, J, Taylor, K, Te, A, Tenbusch, L, Teng, KS, Terakawa, A, Terry, J, Tham, ZD, Tholl, S, Thomas, G, Thong, KM, Tietjen, D, Timadjer, A, Tindall, H, Tipper, S, Tobin, K, Toda, N, Tokuyama, A, Tolibas, M, Tomita, A, Tomita, T, Tomlinson, J, Tonks, L, Topf, J, Topping, S, Torp, A, Torres, A, Totaro, F, Toth, P, Toyonaga, Y, Tripodi, F, Trivedi, K, Tropman, E, Tschope, D, Tse, J, Tsuji, K, Tsunekawa, S, Tsunoda, R, Tucky, B, Tufail, S, Tuffaha, A, Turan, E, Turner, H, Turner, J, Turner, M, Tye, YL, Tyler, A, Tyler, J, Uchi, H, Uchida, H, Uchida, T, Udagawa, T, Ueda, S, Ueda, Y, Ueki, K, Ugni, S, Ugwu, E, Umeno, R, Unekawa, C, Uozumi, K, Urquia, K, Valleteau, A, Valletta, C, van Erp, R, Vanhoy, C, Varad, V, Varma, R, Varughese, A, Vasquez, P, Vasseur, A, Veelken, R, Velagapudi, C, Verdel, K, Vettoretti, S, Vezzoli, G, Vielhauer, V, Viera, R, Vilar, E, Villaruel, S, Vinall, L, Vinathan, 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2024
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3. Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

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Judge, PK, Staplin, N, Mayne, KJ, Wanner, C, Green, JB, Hauske, SJ, Emberson, JR, Preiss, D, Ng, SYA, Roddick, AJ, Sammons, E, Zhu, D, Hill, M, Stevens, W, Wallendszus, K, Brenner, S, Cheung, AK, Liu, ZH, Li, J, Hooi, LS, Liu, WJ, Kadowaki, T, Nangaku, M, Levin, A, Cherney, D, Maggioni, AP, Pontremoli, R, Deo, R, Goto, S, Rossello, X, Tuttle, KR, Steubl, D, Massey, D, Landray, MJ, Baigent, C, Haynes, R, Herrington, WG, Abat, S, Abd Rahman, R, Abdul Cader, R, Abdul Hafidz, MI, Abdul Wahab, MZ, Abdullah, NK, Abdul-Samad, T, Abe, M, Abraham, N, Acheampong, S, Achiri, P, Acosta, JA, Adeleke, A, Adell, V, Adewuyi-Dalton, R, Adnan, N, Africano, A, Agharazii, M, Aguilar, F, Aguilera, A, Ahmad, M, Ahmad, MK, Ahmad, NA, Ahmad, NH, Ahmad, NI, Ahmad Miswan, N, Ahmad Rosdi, H, Ahmed, I, Ahmed, S, Aiello, J, Aitken, A, AitSadi, R, Aker, S, Akimoto, S, Akinfolarin, A, Akram, S, Alberici, F, Albert, C, Aldrich, L, Alegata, M, Alexander, L, Alfaress, S, Alhadj Ali, M, Ali, A, Alicic, R, Aliu, A, Almaraz, R, Almasarwah, R, Almeida, J, Aloisi, A, Al-Rabadi, L, Alscher, D, Alvarez, P, Al-Zeer, B, Amat, M, Ambrose, C, Ammar, H, An, Y, Andriaccio, L, Ansu, K, Apostolidi, A, Arai, N, Araki, H, Araki, S, Arbi, A, Arechiga, O, Armstrong, S, Arnold, T, Aronoff, S, Arriaga, W, Arroyo, J, Arteaga, D, Asahara, S, Asai, A, Asai, N, Asano, S, Asawa, M, Asmee, MF, Aucella, F, Augustin, M, Avery, A, Awad, A, Awang, IY, Awazawa, M, Axler, A, Ayub, W, Azhari, Z, Baccaro, R, Badin, C, Bagwell, B, Bahlmann-Kroll, E, Bahtar, AZ, Bains, D, Bajaj, H, Baker, R, Baldini, E, Banas, B, Banerjee, D, Banno, S, Bansal, S, Barberi, S, Barnes, S, Barnini, C, Barot, C, Barrett, K, Barrios, R, Bartolomei Mecatti, B, Barton, I, Barton, J, Basily, W, Bavanandan, S, Baxter, A, Becker, L, Beddhu, S, Beige, J, Beigh, S, Bell, S, Benck, U, Beneat, A, Bennett, A, Bennett, D, Benyon, S, Berdeprado, J, Bergler, T, Bergner, A, Berry, M, Bevilacqua, M, Bhairoo, J, Bhandari, S, Bhandary, N, Bhatt, A, Bhattarai, M, Bhavsar, M, Bian, W, Bianchini, F, Bianco, S, Bilous, R, Bilton, J, Bilucaglia, D, Bird, C, Birudaraju, D, Biscoveanu, M, Blake, C, Bleakley, N, Bocchicchia, K, Bodine, S, Bodington, R, Boedecker, S, Bolduc, M, Bolton, S, Bond, C, Boreky, F, Boren, K, Bouchi, R, Bough, L, Bovan, D, Bowler, C, Bowman, L, Brar, N, Braun, C, Breach, A, Breitenfeldt, M, Brettschneider, B, Brewer, A, Brewer, G, Brindle, V, Brioni, E, Brown, C, Brown, H, Brown, L, Brown, R, Brown, S, Browne, D, Bruce, K, Brueckmann, M, Brunskill, N, Bryant, M, Brzoska, M, Bu, Y, Buckman, C, Budoff, M, Bullen, M, Burke, A, Burnette, S, Burston, C, Busch, M, Bushnell, J, Butler, S, Büttner, C, Byrne, C, Caamano, A, Cadorna, J, Cafiero, C, Cagle, M, Cai, J, Calabrese, K, Calvi, C, Camilleri, B, Camp, S, Campbell, D, Campbell, R, Cao, H, Capelli, I, Caple, M, Caplin, B, Cardone, A, Carle, J, Carnall, V, Caroppo, M, Carr, S, Carraro, G, Carson, M, Casares, P, Castillo, C, Castro, C, Caudill, B, Cejka, V, Ceseri, M, Cham, L, 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Hamamoto, Y, Hamano, N, Hamm, M, Hanburry, A, Haneda, M, Hanf, C, Hanif, W, Hansen, J, Hanson, L, Hantel, S, Haraguchi, T, Harding, E, Harding, T, Hardy, C, Hartner, C, Harun, Z, Harvill, L, Hasan, A, Hase, H, Hasegawa, F, Hasegawa, T, Hashimoto, A, Hashimoto, C, Hashimoto, M, Hashimoto, S, Haskett, S, Hawfield, A, Hayami, T, Hayashi, M, Hayashi, S, Hazara, A, Healy, C, Hecktman, J, Heine, G, Henderson, H, Henschel, R, Hepditch, A, Herfurth, K, Hernandez, G, Hernandez Pena, A, Hernandez-Cassis, C, Herzog, C, Hewins, S, Hewitt, D, Hichkad, L, Higashi, S, Higuchi, C, Hill, C, Hill, L, Himeno, T, Hing, A, Hirakawa, Y, Hirata, K, Hirota, Y, Hisatake, T, Hitchcock, S, Hodakowski, A, Hodge, W, Hogan, R, Hohenstatt, U, Hohenstein, B, Hooi, L, Hope, S, Hopley, M, Horikawa, S, Hosein, D, Hosooka, T, Hou, L, Hou, W, Howie, L, Howson, A, Hozak, M, Htet, Z, Hu, X, Hu, Y, Huang, J, Huda, N, Hudig, L, Hudson, A, Hugo, C, Hull, R, Hume, L, Hundei, W, Hunt, N, Hunter, A, Hurley, S, Hurst, A, 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Kriatselis, C, Krieger, C, Krish, P, Kruger, B, Ku Md Razi, KR, Kuan, Y, Kubota, S, Kuhn, S, Kumar, P, Kume, S, Kummer, I, Kumuji, R, Küpper, A, Kuramae, T, Kurian, L, Kuribayashi, C, Kurien, R, Kuroda, E, Kurose, T, Kutschat, A, Kuwabara, N, Kuwata, H, La Manna, G, Lacey, M, Lafferty, K, LaFleur, P, Lai, V, Laity, E, Lambert, A, Langlois, M, Latif, F, Latore, E, Laundy, E, Laurienti, D, Lawson, A, Lay, M, Leal, I, Lee, AK, Lee, J, Lee, KQ, Lee, R, Lee, SA, Lee, YY, Lee-Barkey, Y, Leonard, N, Leoncini, G, Leong, CM, Lerario, S, Leslie, A, Lewington, A, Li, N, Li, X, Li, Y, Liberti, L, Liberti, ME, Liew, A, Liew, YF, Lilavivat, U, Lim, SK, Lim, YS, Limon, E, Lin, H, Lioudaki, E, Liu, H, Liu, J, Liu, L, Liu, Q, Liu, X, Liu, Z, Loader, D, Lochhead, H, Loh, CL, Lorimer, A, Loudermilk, L, Loutan, J, Low, CK, Low, CL, Low, YM, Lozon, Z, Lu, Y, Lucci, D, Ludwig, U, Luker, N, Lund, D, Lustig, R, Lyle, S, Macdonald, C, MacDougall, I, Machicado, R, MacLean, D, Macleod, P, Madera, A, Madore, F, 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Miyatsuka, T, Miyazaki, M, Miyazawa, I, Mizumachi, R, Mizuno, M, Moffat, S, Mohamad Nor, FS, Mohamad Zaini, SN, Mohamed Affandi, FA, Mohandas, C, Mohd, R, Mohd Fauzi, NA, Mohd Sharif, NH, Mohd Yusoff, Y, Moist, L, Moncada, A, Montasser, M, Moon, A, Moran, C, Morgan, N, Moriarty, J, Morig, G, Morinaga, H, Morino, K, Morisaki, T, Morishita, Y, Morlok, S, Morris, A, Morris, F, Mostafa, S, Mostefai, Y, Motegi, M, Motherwell, N, Motta, D, Mottl, A, Moys, R, Mozaffari, S, Muir, J, Mulhern, J, Mulligan, S, Munakata, Y, Murakami, C, Murakoshi, M, Murawska, A, Murphy, K, Murphy, L, Murray, S, Murtagh, H, Musa, MA, Mushahar, L, Mustafa, R, Mustafar, R, Muto, M, Nadar, E, Nagano, R, Nagasawa, T, Nagashima, E, Nagasu, H, Nagelberg, S, Nair, H, Nakagawa, Y, Nakahara, M, Nakamura, J, Nakamura, R, Nakamura, T, Nakaoka, M, Nakashima, E, Nakata, J, Nakata, M, Nakatani, S, Nakatsuka, A, Nakayama, Y, Nakhoul, G, Naverrete, G, Navivala, A, Nazeer, I, Negrea, L, Nethaji, C, Newman, E, Ng, TJ, Ngu, LLS, Nimbkar, T, Nishi, H, Nishi, M, Nishi, S, Nishida, Y, Nishiyama, A, Niu, J, Niu, P, Nobili, G, Nohara, N, Nojima, I, Nolan, J, Nosseir, H, Nozawa, M, Nunn, M, Nunokawa, S, Oda, M, Oe, M, Oe, Y, Ogane, K, Ogawa, W, Ogihara, T, Oguchi, G, Ohsugi, M, Oishi, K, Okada, Y, Okajyo, J, Okamoto, S, Okamura, K, Olufuwa, O, Oluyombo, R, Omata, A, Omori, Y, Ong, LM, Ong, YC, Onyema, J, Oomatia, A, Oommen, A, Oremus, R, Orimo, Y, Ortalda, V, Osaki, Y, Osawa, Y, Osmond Foster, J, O'Sullivan, A, Otani, T, Othman, N, Otomo, S, O'Toole, J, Owen, L, Ozawa, T, Padiyar, A, Page, N, Pajak, S, Paliege, A, Pandey, A, Pandey, R, Pariani, H, Park, J, Parrigon, M, Passauer, J, Patecki, M, Patel, M, Patel, R, Patel, T, Patel, Z, Paul, R, Paulsen, L, Pavone, L, Peixoto, A, Peji, J, Peng, BC, Peng, K, Pennino, L, Pereira, E, Perez, E, Pergola, P, Pesce, F, Pessolano, G, Petchey, W, Petr, EJ, Pfab, T, Phelan, P, Phillips, R, Phillips, T, Phipps, M, Piccinni, G, Pickett, T, Pickworth, S, Piemontese, M, Pinto, D, Piper, J, Plummer-Morgan, J, Poehler, D, Polese, L, Poma, V, Postal, A, Pötz, C, Power, A, Pradhan, N, Pradhan, R, Preiss, E, Preston, K, Prib, N, Price, L, Provenzano, C, Pugay, C, Pulido, R, Putz, F, Qiao, Y, Quartagno, R, Quashie-Akponeware, M, Rabara, R, Rabasa-Lhoret, R, Radhakrishnan, D, Radley, M, Raff, R, Raguwaran, S, Rahbari-Oskoui, F, Rahman, M, Rahmat, K, Ramadoss, S, Ramanaidu, S, Ramasamy, S, Ramli, R, Ramli, S, Ramsey, T, Rankin, A, Rashidi, A, Raymond, L, Razali, WAFA, Read, K, Reiner, H, Reisler, A, Reith, C, Renner, J, Rettenmaier, B, Richmond, L, Rijos, D, Rivera, R, Rivers, V, Robinson, H, Rocco, M, Rodriguez-Bachiller, I, Rodriquez, R, Roesch, C, Roesch, J, Rogers, J, Rohnstock, M, Rolfsmeier, S, Roman, M, Romo, A, Rosati, A, Rosenberg, S, Ross, T, Roura, M, Roussel, M, Rovner, S, Roy, S, Rucker, S, Rump, L, Ruocco, M, Ruse, S, Russo, F, Russo, M, Ryder, M, Sabarai, A, Saccà, C, Sachson, R, Sadler, E, Safiee, NS, Sahani, M, Saillant, A, Saini, J, Saito, C, Saito, S, Sakaguchi, K, Sakai, M, Salim, H, Salviani, C, Sampson, A, Samson, F, Sandercock, P, Sanguila, S, Santorelli, G, Santoro, D, Sarabu, N, Saram, T, Sardell, R, Sasajima, H, Sasaki, T, Satko, S, Sato, A, Sato, D, Sato, H, Sato, J, Sato, T, Sato, Y, Satoh, M, Sawada, K, Schanz, M, Scheidemantel, F, Schemmelmann, M, Schettler, E, Schettler, V, Schlieper, GR, Schmidt, C, Schmidt, G, Schmidt, U, Schmidt-Gurtler, H, Schmude, M, Schneider, A, Schneider, I, Schneider-Danwitz, C, Schomig, M, Schramm, T, Schreiber, A, Schricker, S, Schroppel, B, Schulte-Kemna, L, Schulz, E, Schumacher, B, Schuster, A, Schwab, A, Scolari, F, Scott, A, Seeger, W, Segal, M, Seifert, L, Seifert, M, Sekiya, M, Sellars, R, Seman, MR, Shah, S, Shainberg, L, Shanmuganathan, M, Shao, F, Sharma, K, Sharpe, C, Sheikh-Ali, M, Sheldon, J, Shenton, C, Shepherd, A, Shepperd, M, Sheridan, R, Sheriff, Z, Shibata, Y, Shigehara, T, Shikata, K, Shimamura, K, Shimano, H, Shimizu, Y, Shimoda, H, Shin, K, Shivashankar, G, Shojima, N, Silva, R, Sim, CSB, Simmons, K, Sinha, S, Sitter, T, Sivanandam, S, Skipper, M, Sloan, K, Sloan, L, Smith, R, Smyth, J, Sobande, T, Sobata, M, Somalanka, S, Song, X, Sonntag, F, Sood, B, Sor, SY, Soufer, J, Sparks, H, Spatoliatore, G, Spinola, T, Squyres, S, Srivastava, A, Stanfield, J, Staylor, K, Steele, A, Steen, O, Steffl, D, Stegbauer, J, Stellbrink, C, Stellbrink, E, Stevenson, A, Stewart-Ray, V, Stickley, J, Stoffler, D, Stratmann, B, Streitenberger, S, Strutz, F, Stubbs, J, Stumpf, J, Suazo, N, Suchinda, P, Suckling, R, Sudin, A, Sugamori, K, Sugawara, H, Sugawara, K, Sugimoto, D, Sugiyama, H, Sugiyama, T, Sullivan, M, Sumi, M, Suresh, N, Sutton, D, Suzuki, H, Suzuki, R, Suzuki, Y, Swanson, E, Swift, P, Syed, S, Szerlip, H, Taal, M, Taddeo, M, Tailor, C, Tajima, K, Takagi, M, Takahashi, K, Takahashi, M, Takahashi, T, Takahira, E, Takai, T, Takaoka, M, Takeoka, J, Takesada, A, Takezawa, M, Talbot, M, Taliercio, J, Talsania, T, Tamori, Y, Tamura, R, Tamura, Y, Tan, CHH, Tan, EZZ, Tanabe, A, Tanabe, K, Tanaka, A, Tanaka, N, Tang, S, Tang, Z, Tanigaki, K, Tarlac, M, Tatsuzawa, A, Tay, JF, Tay, LL, Taylor, J, Taylor, K, Te, A, Tenbusch, L, Teng, KS, Terakawa, A, Terry, J, Tham, ZD, Tholl, S, Thomas, G, Thong, KM, Tietjen, D, Timadjer, A, Tindall, H, Tipper, S, Tobin, K, Toda, N, Tokuyama, A, Tolibas, M, Tomita, A, Tomita, T, Tomlinson, J, Tonks, L, Topf, J, Topping, S, Torp, A, Torres, A, Totaro, F, Toth, P, Toyonaga, Y, Tripodi, F, Trivedi, K, Tropman, E, Tschope, D, Tse, J, Tsuji, K, Tsunekawa, S, Tsunoda, R, Tucky, B, Tufail, S, Tuffaha, A, Turan, E, Turner, H, Turner, J, Turner, M, Tye, YL, Tyler, A, Tyler, J, Uchi, H, Uchida, H, Uchida, T, Udagawa, T, Ueda, S, Ueda, Y, Ueki, K, Ugni, S, Ugwu, E, Umeno, R, Unekawa, C, Uozumi, K, Urquia, K, Valleteau, A, Valletta, C, van Erp, R, Vanhoy, C, Varad, V, Varma, R, Varughese, A, Vasquez, P, Vasseur, A, Veelken, R, Velagapudi, C, Verdel, K, Vettoretti, S, Vezzoli, G, Vielhauer, V, Viera, R, Vilar, E, Villaruel, S, Vinall, L, Vinathan, J, Visnjic, M, Voigt, E, von-Eynatten, M, Vourvou, M, Wada, J, Wada, T, Wada, Y, Wakayama, K, Wakita, Y, Walters, T, Wan Mohamad, WH, Wang, L, Wang, W, Wang, X, Wang, Y, Wanninayake, S, Watada, H, Watanabe, K, Watanabe, M, Waterfall, H, Watkins, D, Watson, S, Weaving, L, Weber, B, Webley, Y, Webster, A, Webster, M, Weetman, M, Wei, W, Weihprecht, H, Weiland, L, Weinmann-Menke, J, Weinreich, T, Wendt, R, Weng, Y, Whalen, M, Whalley, G, Wheatley, R, Wheeler, A, Wheeler, J, Whelton, P, White, K, Whitmore, B, Whittaker, S, Wiebel, J, Wiley, J, Wilkinson, L, Willett, M, Williams, A, Williams, E, Williams, K, Williams, T, Wilson, A, Wilson, P, Wincott, L, Wines, E, Winkelmann, B, Winkler, M, Winter-Goodwin, B, Witczak, J, Wittes, J, Wittmann, M, Wolf, G, Wolf, L, Wolfling, R, Wong, C, Wong, E, Wong, HS, Wong, LW, Wong, YH, Wonnacott, A, Wood, A, Wood, L, Woodhouse, H, Wooding, N, Woodman, A, Wren, K, Wu, J, Wu, P, Xia, S, Xiao, H, Xiao, X, Xie, Y, Xu, C, Xu, Y, Xue, H, Yahaya, H, Yalamanchili, H, Yamada, A, Yamada, N, Yamagata, K, Yamaguchi, M, Yamaji, Y, Yamamoto, A, Yamamoto, S, Yamamoto, T, Yamanaka, A, Yamano, T, Yamanouchi, Y, Yamasaki, N, Yamasaki, Y, Yamashita, C, Yamauchi, T, Yan, Q, Yanagisawa, E, Yang, F, Yang, L, Yano, S, Yao, S, Yao, Y, Yarlagadda, S, Yasuda, Y, Yiu, V, Yokoyama, T, Yoshida, S, Yoshidome, E, Yoshikawa, H, Young, A, Young, T, Yousif, V, Yu, H, Yu, Y, Yuasa, K, Yusof, N, Zalunardo, N, Zander, B, Zani, R, Zappulo, F, Zayed, M, Zemann, B, Zettergren, P, Zhang, H, Zhang, L, Zhang, N, Zhang, X, Zhao, J, Zhao, L, Zhao, S, Zhao, Z, Zhong, H, Zhou, N, Zhou, S, Zhu, L, Zhu, S, Zietz, M, Zippo, M, Zirino, F, and Zulkipli, FH

Published
2024
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5. Dimethyl fumarate and 4-octyl itaconate are anticoagulants that suppress Tissue Factor in macrophages via inhibition of Type I Interferon

Author

Ryan, Tristram A. J., Hooftman, Alexander, Rehill, Aisling M., Johansen, Matt D., Brien, Eóin C. O’, Toller-Kawahisa, Juliana E., Wilk, Mieszko M., Day, Emily A., Weiss, Hauke J., Sarvari, Pourya, Vozza, Emilio G., Schramm, Fabian, Peace, Christian G., Zotta, Alessia, Miemczyk, Stefan, Nalkurthi, Christina, Hansbro, Nicole G., McManus, Gavin, O’Doherty, Laura, Gargan, Siobhan, Long, Aideen, Dunne, Jean, Cheallaigh, Clíona Ní, Conlon, Niall, Carty, Michael, Fallon, Padraic G., Mills, Kingston H. G., Creagh, Emma M., Donnell, James S. O’, Hertzog, Paul J., Hansbro, Philip M., McLoughlin, Rachel M., Wygrecka, Małgorzata, Preston, Roger J. S., Zasłona, Zbigniew, and O’Neill, Luke A. J.

Published
2023
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6. Publisher Correction: Dimethyl fumarate and 4-octyl itaconate are anticoagulants that suppress Tissue Factor in macrophages via inhibition of Type I Interferon

Author

Ryan, Tristram A. J., Hooftman, Alexander, Rehill, Aisling M., Johansen, Matt D., O’ Brien, Eóin C., Toller-Kawahisa, Juliana E., Wilk, Mieszko M., Day, Emily A., Weiss, Hauke J., Sarvari, Pourya, Vozza, Emilio G., Schramm, Fabian, Peace, Christian G., Zotta, Alessia, Miemczyk, Stefan, Nalkurthi, Christina, Hansbro, Nicole G., McManus, Gavin, O’Doherty, Laura, Gargan, Siobhan, Long, Aideen, Dunne, Jean, Cheallaigh, Clíona Ní, Conlon, Niall, Carty, Michael, Fallon, Padraic G., Mills, Kingston H. G., Creagh, Emma M., O’ Donnell, James S., Hertzog, Paul J., Hansbro, Philip M., McLoughlin, Rachel M., Wygrecka, Małgorzata, Preston, Roger J. S., Zasłona, Zbigniew, and O’Neill, Luke A. J.

Published
2023
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10. The circadian clock influences T cell responses to vaccination by regulating dendritic cell antigen processing

Author

Mariana P. Cervantes-Silva, Richard G. Carroll, Mieszko M. Wilk, Diana Moreira, Cloe A. Payet, James R. O’Siorain, Shannon L. Cox, Lauren E. Fagan, Paula A. Klavina, Yan He, Tabea Drewinski, Alan McGinley, Sharleen M. Buel, George A. Timmons, James O. Early, Roger J. S. Preston, Jennifer M. Hurley, David K. Finlay, Ingmar Schoen, F. Javier Sánchez-García, Kingston H. G. Mills, and Annie M. Curtis

Subjects
Science
Abstract

Circadian rhythms are known to impact a range of biological processes including in the immune system. Here the authors show how circadian rhythms modulate the T cell response to vaccination via regulation of dendritic cell metabolism.

Published
2022
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12. Caspase-11 promotes allergic airway inflammation

Author

Zbigniew Zasłona, Ewelina Flis, Mieszko M. Wilk, Richard G. Carroll, Eva M. Palsson-McDermott, Mark M. Hughes, Ciana Diskin, Kathy Banahan, Dylan G. Ryan, Alexander Hooftman, Alicja Misiak, Jay Kearney, Gunter Lochnit, Wilhelm Bertrams, Timm Greulich, Bernd Schmeck, Oliver J. McElvaney, Kingston H. G. Mills, Ed C. Lavelle, Małgorzata Wygrecka, Emma M. Creagh, and Luke A. J. O’Neill

Subjects
Science
Abstract

Caspase 11 activation involves transcriptional upregulation and proteolytic cleavage. Here the authors show that prostaglandin E2 prevents caspase-11-mediated pyroptosis, blocking caspase-11 mRNA and protein upregulation in macrophages and in vivo, and that mice lacking caspase-11 are strongly protected from allergic airway inflammation.

Published
2020
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14. The Effects of Trained Innate Immunity on T Cell Responses; Clinical Implications and Knowledge Gaps for Future Research

Author

Dearbhla M. Murphy, Kingston H. G. Mills, and Sharee A. Basdeo

Subjects
trained immunity, T cells, adaptive, innate, BCG, beta-glucan, Immunologic diseases. Allergy, RC581-607
Abstract

The burgeoning field of innate immune training, also called trained immunity, has given immunologists new insights into the role of innate responses in protection against infection and in modulating inflammation. Moreover, it has led to a paradigm shift in the way we think about immune memory and the interplay between innate and adaptive immune systems in conferring immunity against pathogens. Trained immunity is the term used to describe the medium-term epigenetic and metabolic reprogramming of innate immune cells in peripheral tissues or in the bone marrow stem cell niche. It is elicited by an initial challenge, followed by a significant period of rest that results in an altered response to a subsequent, unrelated challenge. Trained immunity can be associated with increased production of proinflammatory mediators, such as IL-1β, TNF and IL-6, and increased expression of markers on innate immune cells associated with antigen presentation to T cells. The microenvironment created by trained innate immune cells during the secondary challenge may have profound effects on T cell responses, such as altering the differentiation, polarisation and function of T cell subtypes, including Th17 cells. In addition, the Th1 cytokine IFN-γ plays a critical role in establishing trained immunity. In this review, we discuss the evidence that trained immunity impacts on or can be impacted by T cells. Understanding the interplay between innate immune training and how it effects adaptive immunity will give insights into how this phenomenon may affect the development or progression of disease and how it could be exploited for therapeutic interventions or to enhance vaccine efficacy.

Published
2021
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20. Loss of the molecular clock in myeloid cells exacerbates T cell-mediated CNS autoimmune disease

Author

Caroline E. Sutton, Conor M. Finlay, Mathilde Raverdeau, James O. Early, Joseph DeCourcey, Zbigniew Zaslona, Luke A. J. O’Neill, Kingston H. G. Mills, and Annie M. Curtis

Subjects
Science
Abstract

Circadian controls of immune responses by the molecular clock have been reported, but the underlying mechanisms are unclear. Here the authors show that the master circadian gene, Bmal1, is essential for modulating the homeostasis of myeloid cells to control pro-inflammatory IL-17+/IFN-γ+ T cells in autoimmunity.

Published
2017
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21. Recombinant BCG Expressing LTAK63 Adjuvant induces Superior Protection against Mycobacterium tuberculosis

Author

Ivan P. Nascimento, Dunia Rodriguez, Carina C. Santos, Eduardo P. Amaral, Henrique K. Rofatto, Ana P. Junqueira-Kipnis, Eduardo D. C. Gonçalves, Maria R. D’Império-Lima, Mario H. Hirata, Celio L. Silva, Nathalie Winter, Brigitte Gicquel, Kingston H. G. Mills, Mariagrazia Pizza, Rino Rappuoli, and Luciana C. C. Leite

Subjects
Medicine, Science
Abstract

Abstract In order to develop an improved BCG vaccine against tuberculosis we have taken advantage of the adjuvant properties of a non-toxic derivative of Escherichia coli heat labile enterotoxin (LT), LTAK63. We have constructed rBCG strains expressing LTAK63 at different expression levels. Mice immunized with BCG expressing low levels of LTAK63 (rBCG-LTAK63lo) showed higher Th1 cytokines and IL-17 in the lungs, and when challenged intratracheally with Mycobacterium tuberculosis displayed a 2.0–3.0 log reduction in CFU as compared to wild type BCG. Histopathological analysis of lung tissues from protected mice revealed a reduced inflammatory response. Immunization with rBCG-LTAK63lo also protected against a 100-fold higher challenge dose. Mice immunized with rBCG-LTAK63lo produced an increase in TGF-β as compared with BCG after challenge, with a corresponding reduction in Th1 and Th17 cytokines, as determined by Real Time RT-PCR. Furthermore, rBCG-LTAK63lo also displays protection against challenge with a highly virulent Beijing isolate. Our findings suggest that BCG with low-level expression of the LTAK63 adjuvant induces a stronger immune response in the lungs conferring higher levels of protection, and a novel mechanism subsequently triggers a regulatory immune response, which then limits the pathology. The rBCG-LTAK63lo strain can be the basis of an improved vaccine against tuberculosis.

Published
2017
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22. UCP3 reciprocally controls CD4+ Th17 and Treg cell differentiation.

Author

Emma B O'Connor, Natalia Muñoz-Wolf, Gemma Leon, Ed C Lavelle, Kingston H G Mills, Patrick T Walsh, and Richard K Porter

Subjects
Medicine, Science
Abstract

Uncoupling proteins (UCPs) are members of the mitochondrial anion carrier superfamily that can mediate the transfer of protons into the mitochondrial matrix from the intermembrane space. We have previously reported UCP3 expression in thymocytes, mitochondria of total splenocytes and splenic lymphocytes. Here, we demonstrate that Ucp3 is expressed in peripheral naive CD4+ T cells at the mRNA level before being markedly downregulated following activation. Non-polarized, activated T cells (Th0 cells) from Ucp3-/- mice produced significantly more IL-2, had increased expression of CD25 and CD69 and were more proliferative than Ucp3+/+ Th0 cells. The altered IL-2 expression observed between T cells from Ucp3+/+ and Ucp3-/- mice may be a factor in determining differentiation into Th17 or induced regulatory (iTreg) cells. When compared to Ucp3+/+, CD4+ T cells from Ucp3-/- mice had increased FoxP3 expression under iTreg conditions. Conversely, Ucp3-/- CD4+ T cells produced a significantly lower concentration of IL-17A under Th17 cell-inducing conditions in vitro. These effects were mirrored in antigen-specific T cells from mice immunized with KLH and CT. Interestingly, the altered responses of Ucp3-/- T cells were partially reversed upon neutralisation of IL-2. Together, these data indicate that UCP3 acts to restrict the activation of naive T cells, acting as a rheostat to dampen signals following TCR and CD28 co-receptor ligation, thereby limiting early activation responses. The observation that Ucp3 ablation alters the Th17:Treg cell balance in vivo as well as in vitro suggests that UCP3 is a potential target for the treatment of Th17 cell-mediated autoimmune diseases.

Published
2020
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23. Anti-inflammatory Trained Immunity Mediated by Helminth Products Attenuates the Induction of T Cell-Mediated Autoimmune Disease

Author

Shauna M. Quinn, Kyle Cunningham, Mathilde Raverdeau, Robert J. Walsh, Lucy Curham, Anna Malara, and Kingston H. G. Mills

Subjects
trained immunity, innate immune memory, macrophages, autoimmune disease, EAE, Th17 cells, Immunologic diseases. Allergy, RC581-607
Abstract

Recent studies have suggested that the innate immune system can display characteristics of immunological memory and this has been called “innate immune memory” or “trained immunity.” Certain fungal products have been shown to induce epigenetic imprinting on monocytes/macrophages that results in heightened inflammatory responses to subsequent stimuli. Here we report that innate immune cells can be trained to be more anti-inflammatory following exposure to products of a helminth pathogen. Macrophages trained in vitro with Fasciola hepatica total extract (FHTE) had enhanced IL-10 and IL-1RA, but reduced TNF production upon re-stimulation with FHTE or TLR ligands and this was reversed by inhibitors of DNA methylation. In contrast, macrophages trained with β-glucan or Bacillus Calmette–Guérin had enhanced TNF production upon re-stimulation with Pam3cys or LPS. Furthermore, FHTE-trained macrophages had enhanced expression of markers of alternative activated macrophages (AAM). Macrophages from mice treated with FHTE expressed markers of AAM and had heightened IL-10 and IL-1RA production in response to FHTE or TLR ligands and had suppressed TNF and IL-12p40 production. Macrophages from mice treated with FHTE had reduced APC function and inhibited IL-17 production and the encephalitogenic activity of T cells in the experimental autoimmune encephalomyelitis (EAE) model. In addition, mice pre-treated with FHTE were resistant to induction of EAE and this was associated with a significant reduction in IL-17-producing γδ and CD4 T cells infiltrating the CNS. Our findings reveal that cells of the innate immune system can be trained in vitro or in vivo to be more anti-inflammatory by exposure to helminth products and this protects mice against the induction of a T cell-mediated autoimmune disease.

Published
2019
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24. A Pertussis Outer Membrane Vesicle-Based Vaccine Induces Lung-Resident Memory CD4 T Cells and Protection Against Bordetella pertussis, Including Pertactin Deficient Strains

Author

María Eugenia Zurita, Mieszko M. Wilk, Francisco Carriquiriborde, Erika Bartel, Griselda Moreno, Alicja Misiak, Kingston H. G. Mills, and Daniela Hozbor

Subjects
Bordetella pertussis, pertussis, outer membrane vesicles, TRM cells, pertactin deficient strains, protection, Microbiology, QR1-502
Abstract

Pertussis is a respiratory infectious disease that has been resurged during the last decades. The change from the traditional multi-antigen whole-cell pertussis (wP) vaccines to acellular pertussis (aP) vaccines that consist of a few antigens formulated with alum, appears to be a key factor in the resurgence of pertussis in many countries. Though current aP vaccines have helped to reduce the morbidity and mortality associated with pertussis, they do not provide durable immunity or adequate protection against the disease caused by the current circulating strains of Bordetella pertussis, which have evolved in the face of the selection pressure induced by the vaccines. Based on the hypothesis that a new vaccine containing multiple antigens could overcome deficiencies in the current aP vaccines, we have designed and characterized a vaccine candidate based on outer membrane vesicle (OMVs). Here we show that the OMVs vaccine, but not an aP vaccine, protected mice against lung infection with a circulating pertactin (PRN)-deficient isolate. Using isogenic bacteria that in principle only differ in PRN expression, we found that deficiency in PRN appears to be largely responsible for the failure of the aP vaccine to protect against this circulating clinical isolates. Regarding the durability of induced immunity, we have already reported that the OMV vaccine is able to induce long-lasting immune responses that effectively prevent infection with B. pertussis. Consistent with this, here we found that CD4 T cells with a tissue-resident memory (TRM) cell phenotype (CD44+CD62LlowCD69+ and/or CD103+) accumulated in the lungs of mice 14 days after immunization with 2 doses of the OMVs vaccine. CD4 TRM cells, which have previously been shown to play a critical role sustained protective immunity against B. pertussis, were also detected in mice immunized with wP vaccine, but not in the animals immunized with a commercial aP vaccine. The CD4 TRM cells secreted IFN-γ and IL-17 and were significantly expanded through local proliferation following respiratory challenge of mice with B. pertussis. Our findings that the OMVs vaccine induce respiratory CD4 TRM cells may explain the ability of this vaccine to induce long-term protection and is therefore an ideal candidate for a third generation vaccine against B. pertussis.

Published
2019
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26. Targeting the NLRP3 inflammasome reduces inflammation in hidradenitis suppurativa skin

Author

Moran, Barry, primary, Smith, Conor M, additional, Zabarowski, Alexandra, additional, Ryan, Mark, additional, Karman, Jozsef, additional, Dunstan, Robert W, additional, Smith, Kathleen M, additional, Hambly, Roisin, additional, Musilova, Jana, additional, Petrasca, Andreea, additional, Fabre, Aurelie, additional, O’Donnell, Margaret, additional, Hokamp, Karsten, additional, Mills, Kingston H G, additional, Housley, William J, additional, Winter, Desmond C, additional, Kirby, Brian, additional, and Fletcher, Jean M, additional

Published
2023
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27. Targeting the NLRP3 inflammasome reduces inflammation in hidradenitis suppurativa skin

Author

Barry Moran, Conor M Smith, Alexandra Zabarowski, Mark Ryan, Jozsef Karman, Robert W Dunstan, Kathleen M Smith, Roisin Hambly, Jana Musilova, Andreea Petrasca, Aurelie Fabre, Margaret O’Donnell, Karsten Hokamp, Kingston H G Mills, William J Housley, Desmond C Winter, Brian Kirby, and Jean M Fletcher

Subjects
Dermatology
Abstract

Background Treatment for the debilitating disease hidradenitis suppurativa (HS) is inadequate in many patients. Despite an incidence of approximately 1%, HS is often underrecognized and underdiagnosed and is associated with a high morbidity and poor quality of life. Objectives A better understanding of its pathogenesis is required to design new therapeutic strategies. Methods In this study we employed single cell RNA sequencing to analyse gene expression in immune cells isolated from involved HS skin compared with healthy skin. Flow cytometry was used to quantify the absolute numbers of the main immune populations. Secretion of inflammatory mediators from skin explant cultures was measured using multiplex assays and ELISA. Results Single cell RNA sequencing analysis identified a significant enrichment in the frequency of plasma cells, Th17 cells and dendritic cell subsets in HS skin, and the immune transcriptome was distinct and much more heterogenous when compared with healthy skin. Flow cytometry revealed significantly increased numbers of T cells, B cells, neutrophils, dermal macrophages, and dendritic cells into involved HS skin. Genes and pathways associated with Th17 cells, IL-17, IL-1β, and the NLRP3 inflammasome were enhanced in HS skin, particularly in samples with a high inflammatory load. Inflammasome constituent genes principally mapped to Langerhans cells and a subpopulation of dendritic cells. The secretome of HS skin explants contained significantly increased concentrations of inflammatory mediators including IL-1β and IL-17A, and culture with an NLRP3 inflammasome inhibitor significantly reduced the secretion of these as well as other key mediators of inflammation. Conclusions These data provide a rationale for targeting the NLRP3 inflammasome in HS using small molecule inhibitors which are currently being tested for other indications.

Published
2023
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28. A guiding map for inflammation

Author

Netea, Mihai G, Balkwill, Frances, Chonchol, Michel, Cominelli, Fabio, Donath, Marc Y, Giamarellos-Bourboulis, Evangelos J, Golenbock, Douglas, Gresnigt, Mark S, Heneka, Michael T, Hoffman, Hal M, Hotchkiss, Richard, Joosten, Leo A B, Kastner, Daniel L, Korte, Martin, Latz, Eicke, Libby, Peter, Mandrup-Poulsen, Thomas, Mantovani, Alberto, Mills, Kingston H G, Nowak, Kristen L, O'Neill, Luke A, Pickkers, Peter, van der Poll, Tom, Ridker, Paul M, Schalkwijk, Joost, Schwartz, David A, Siegmund, Britta, Steer, Clifford J, Tilg, Herbert, van der Meer, Jos W M, van de Veerdonk, Frank L, and Dinarello, Charles A

Published
2017
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30. CD4 TRM Cells Following Infection and Immunization: Implications for More Effective Vaccine Design

Author

Mieszko M. Wilk and Kingston H. G. Mills

Subjects
memory CD4 T cell, tissue-resident memory T cell, infection, immunization, vaccine, protective immunity, Immunologic diseases. Allergy, RC581-607
Abstract

The induction of immunological memory, which is mediated by memory T and B cells, is central to adaptive protective immunity to pathogens induced by previous infection and is the cornerstone of effective vaccine design. Recent studies in mice have suggested that memory T cells that accumulate in tissues, termed tissue-resident memory T (TRM) cells, play a crucial role in maintaining long-term protective immunity to mucosal pathogens. CD4 and CD8 TRM cells can be induced following infection at mucosal sites or the skin, where they are maintained and poised to respond rapidly to reinfection with the same pathogen. TRM cells can also be generated by vaccination, but their induction is influenced by a number of factors, including the type of vaccine, the adjuvant, and the route of immunization. Live attenuated vaccines appear to be more effective than killed or subunit vaccines at inducing TRM cells and mucosal immunization, especially by intranasal route, is more effective than parenteral delivery. However, evidence is emerging that formulation of killed or subunit vaccines with novel adjuvants, especially those that generate Th1 and Th17 responses, can promote the induction of TRM cells. While TRM cells are also present at high number in mucosal tissues in humans, one of the challenge will be to develop methodologies for routine quantification of these cells in humans. Nevertheless, the identification of approaches for optimum induction of TRM cells in mice should assist in the design of more effective vaccines that sustain protective immunity against a range of human pathogens.

Published
2018
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31. Azithromycin Clears Bordetella pertussis Infection in Mice but Also Modulates Innate and Adaptive Immune Responses and T Cell Memory

Author

Lisa Borkner, Alicja Misiak, Mieszko M. Wilk, and Kingston H. G. Mills

Subjects
Bordetella pertussis, macrolide antibiotic, immune modulation, Th1/Th17 cell, innate immunity, memory T cells, Immunologic diseases. Allergy, RC581-607
Abstract

Treatment with the macrolide antibiotic azithromycin (AZM) is an important intervention for controlling infection of children with Bordetella pertussis and as a prophylaxis for preventing transmission to family members. However, antibiotics are known to have immunomodulatory effects independent of their antimicrobial activity. Here, we used a mouse model to examine the effects of AZM treatment on clearance of B. pertussis and induction of innate and adaptive immunity. We found that treatment of mice with AZM either 7 or 14 days post challenge effectively cleared the bacteria from the lungs. The numbers of innate immune cells in the lungs were significantly reduced in antibiotic-treated mice. Furthermore, AZM reduced the activation status of macrophages and dendritic cells, but only in mice treated on day 7. Early treatment with antibiotics also reduced the frequency of tissue-resident T cells and IL-17-producing cells in the lungs. To assess the immunomodulatory effects of AZM independent of its antimicrobial activity, mice were antibiotic treated during immunization with a whole cell pertussis (wP) vaccine. Protection against B. pertussis induced by immunization with wP was slightly reduced in AZM-treated mice. Antibiotic-treated wP-immunized mice had reduced numbers of lung-resident memory CD4 T cells and IL-17-production and reduced CD49d expression on splenic CD4 T cells after challenge, suggestive of impaired CD4 T cell memory. Taken together these results suggest that AZM can modulate the induction of memory CD4 T cells during B. pertussis infection, but this may in part be due to the clearance of B. pertussis and resulting loss of components that stimulate innate and adaptive immune response.

Published
2018
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32. Author Correction: A guiding map for inflammation

Author

Netea, Mihai G., Balkwill, Frances, Chonchol, Michel, Cominelli, Fabio, Donath, Marc Y., Giamarellos-Bourboulis, Evangelos J., Golenbock, Douglas, Gresnigt, Mark S., Heneka, Michael T., Hoffman, Hal M., Hotchkiss, Richard, Joosten, Leo A. B., Kastner, Daniel L., Korte, Martin, Latz, Eicke, Libby, Peter, Mandrup-Poulsen, Thomas, Mantovani, Alberto, Mills, Kingston H. G., Nowak, Kristen L., O’Neill, Luke A., Pickkers, Peter, van der Poll, Tom, Ridker, Paul M., Schalkwijk, Joost, Schwartz, David A., Siegmund, Britta, Steer, Clifford J., Tilg, Herbert, van der Meer, Jos W. M., van de Veerdonk, Frank L., and Dinarello, Charles A.

Published
2021
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38. Modified Bacterial Toxins

Author

Lavelle, Ed C., Leavy, Olive, Mills, Kingston H. G., St. Georgiev, Vassil, editor, Hackett, Charles J., editor, and Harn, Donald A., Jr., editor

Published
2006
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39. Pyruvate Kinase M2 Is Required for the Expression of the Immune Checkpoint PD-L1 in Immune Cells and Tumors

Author

Eva M. Palsson-McDermott, Lydia Dyck, Zbigniew Zasłona, Deepthi Menon, Anne F. McGettrick, Kingston H. G. Mills, and Luke A. O’Neill

Subjects
PD-L1, pyruvate kinase isoform M2, LPS, macrophages, dendritic cells, tumor cells, Immunologic diseases. Allergy, RC581-607
Abstract

Blocking interaction of the immune checkpoint receptor PD-1 with its ligand PD-L1 is associated with good clinical outcomes in a broad variety of malignancies. High levels of PD-L1 promote tumor growth by restraining CD8+ T-cell responses against tumors. Limiting PD-L1 expression and function is therefore critical for allowing the development of antitumor immune responses and effective tumor clearance. Pyruvate kinase isoform M2 (PKM2) is also a key player in regulating cancer as well as immune responses. PKM2 catalyzes the final rate-limiting step of glycolysis. Furthermore, PKM2 as a dimer translocates to the nucleus, where it stimulates hypoxia-inducible factor 1α (Hif-1α) transactivation domain function and recruitment of p300 to the hypoxia response elements (HRE) of Hif-1α target genes. Here, we provide the first evidence of a role for PKM2 in regulating the expression of PD-L1 on macrophages, dendritic cells (DCs), T cells, and tumor cells. LPS-induced expression of PD-L1 in primary macrophages was inhibited by the PKM2 targeting compound TEPP-46. Furthermore, RNA silencing of PKM2 inhibited LPS-induced PD-L1 expression. This regulation occurs through direct binding of PKM2 and Hif-1α to HRE sites on the PD-L1 promoter. Moreover, TEPP-46 inhibited expression of PD-L1 on macrophages, DCs, and T cells as well as tumor cells in a mouse CT26 cancer model. These findings broaden our understanding of how PKM2 may contribute to tumor progression and may explain the upregulation of PD-L1 in the tumor microenvironment.

Published
2017
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41. The circadian clock influences T cell responses to vaccination by regulating dendritic cell antigen processing

Author

Cervantes-Silva, Mariana P., primary, Carroll, Richard G., additional, Wilk, Mieszko M., additional, Moreira, Diana, additional, Payet, Cloe A., additional, O’Siorain, James R., additional, Cox, Shannon L., additional, Fagan, Lauren E., additional, Klavina, Paula A., additional, He, Yan, additional, Drewinski, Tabea, additional, McGinley, Alan, additional, Buel, Sharleen M., additional, Timmons, George A., additional, Early, James O., additional, Preston, Roger J. S., additional, Hurley, Jennifer M., additional, Finlay, David K., additional, Schoen, Ingmar, additional, Javier Sánchez-García, F., additional, Mills, Kingston H. G., additional, and Curtis, Annie M., additional

Published
2022
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45. IL-33–Stimulated Murine Mast Cells Polarize Alternatively Activated Macrophages, Which Suppress T Cells That Mediate Experimental Autoimmune Encephalomyelitis

Author

Benjamin Doyle, Kingston H. G. Mills, Conor M. Finlay, and Kyle T. Cunningham

Subjects
Cell type, Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis, T-Lymphocytes, Immunology, Cell, Mice, 03 medical and health sciences, 0302 clinical medicine, Immune system, Downregulation and upregulation, Immune Tolerance, medicine, Animals, Humans, Immunology and Allergy, Macrophage, Mast Cells, Mice, Knockout, Chemistry, Macrophages, Innate lymphoid cell, Experimental autoimmune encephalomyelitis, Cell Differentiation, Macrophage Activation, Interleukin-33, medicine.disease, Cell biology, Mice, Inbred C57BL, Interleukin 33, Disease Models, Animal, medicine.anatomical_structure, Female, 030215 immunology
Abstract

IL-33 is known to promote type 2 immune responses through ST2, a component of the IL-33R complex, expressed primarily on mast cells, Th2 cells, group 2 innate lymphoid cells and regulatory T cells, and to a lesser extent, on NK cells and Th1 cells. Consistent with previous studies, we found that IL-33 polarized alternatively activated macrophages (AAMΦ) in vivo. However, in vitro stimulation of murine bone marrow–derived or peritoneal macrophages with IL-33 failed to promote arginase activity or expression of YM-1 or Retnla, markers of AAMΦ. Furthermore, macrophages have low/no basal expression of ST2. This suggested that alternative activation of macrophages may involve an IL-33–responsive third-party cell. Because mast cells have the highest expression of ST2 relative to other leukocytes, we focused on this cell type. Coculture experiments showed that IL-33–stimulated mast cells polarized AAMΦ through production of soluble factors. IL-33–stimulated mast cells produced a range of cytokines, including IL-6 and IL-13. Mast cell–derived IL-13 was required for induction of AAMΦ, whereas mast cell–derived IL-6 enhanced macrophage responsiveness to IL-13 via upregulation of the IL-4Rα receptor. Furthermore, we found that AAMΦ polarized by IL-33–stimulated mast cells could suppress proliferation and IL-17 and IFN-γ production by T cells. Finally, we show that AAMΦ polarized by IL-33–stimulated mast cells attenuated the encephalitogenic function of T cells in the experimental autoimmune encephalomyelitis model. Our findings reveal that IL-33 can promote immunosuppressive responses by polarizing AAMΦ via mast cell–derived IL-6 and IL-13.

Published
2020
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46. Overcoming Waning Immunity in Pertussis Vaccines: Workshop of the National Institute of Allergy and Infectious Diseases

Author

Kristina T. Lu, Robert C. Read, Nicola P. Klein, Eric T. Harvill, Pejman Rohani, Marcela F. Pasetti, Kathryn M. Edwards, Peter Sebo, Xin-Xing Gu, F. Heath Damron, Purnima Dubey, Kingston H. G. Mills, and Mariette Barbier

Subjects
Bordetella pertussis, medicine.medical_specialty, Allergy, Whooping Cough, Immunology, Acellular pertussis vaccines, Article, 03 medical and health sciences, Vaccines, Acellular, 0302 clinical medicine, National Institute of Allergy and Infectious Diseases (U.S.), Immunity, medicine, Animals, Humans, Immunology and Allergy, Waning immunity, Intensive care medicine, Pertussis Vaccine, biology, Transmission (medicine), business.industry, Public health, biology.organism_classification, medicine.disease, United States, Acellular vaccines, business, 030215 immunology
Abstract

Despite high vaccine coverage in many parts of the world, pertussis is resurging in a number of areas in which acellular vaccines are the primary vaccine administered to infants and young children. This is attributed in part to the suboptimal and short-lived immunity elicited by acellular pertussis vaccines and to their inability to prevent nasal colonization and transmission of the etiologic agent Bordetella pertussis. In response to this escalating public health concern, the National Institute of Allergy and Infectious Diseases held the workshop “Overcoming Waning Immunity in Pertussis Vaccines” in September 2019 to identify issues and possible solutions for the defects in immunity stimulated by acellular pertussis vaccines. Discussions covered aspects of the current problem, gaps in knowledge and possible paths forward. This review summarizes presentations and discussions of some of the key points that were raised by the workshop.

Published
2020
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47. Exercise-induced re-programming of age-related metabolic changes in microglia is accompanied by a reduction in senescent cells

Author

Marina A. Lynch, Virginia Mela, Kingston H. G. Mills, Mark Milner, Bibiana C Mota, Áine M. Kelly, and Aoife M. McGinley

Subjects
0301 basic medicine, Aging, medicine.medical_specialty, Phosphofructokinase-2, Phagocytosis, Immunology, Mice, 03 medical and health sciences, Behavioral Neuroscience, 0302 clinical medicine, Physical Conditioning, Animal, Age related, Internal medicine, medicine, Animals, Glycolysis, Treadmill, Novel object recognition, Cellular Senescence, Neuroinflammation, Microglia, Endocrine and Autonomic Systems, business.industry, Brain, Master regulator, Cellular Reprogramming, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, business, 030217 neurology & neurosurgery
Abstract

Microglial activation and neuroinflammatory changes are characteristic of the aged brain and contribute to age-related cognitive impairment. Exercise improves cognitive function in aged animals, perhaps because of a modulatory effect on microglial activation. Recent evidence indicates that inflammatory microglia are glycolytic, driven by an increase in 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), an enzyme that is described as the master regulator of glycolysis. Here we investigated whether microglia from aged animals exhibited a glycolytic signature and whether exercise exerted a modulatory effect on this metabolic profile. Young (4 month-old) and aged (18 month-old) mice were trained for 10 days on a treadmill. One day before sacrifice, animals were assessed in the novel object recognition and the object displacement tests. Animals were sacrificed after the last bout of exercise, microglial cells were isolated, cultured for 5 days and assessed for metabolic profile. Performance in both behavioural tests was impaired in sedentary aged animals and exercise attenuated this age-related effect. A significant increase in glycolysis, glycolytic capacity and PFKFB3 was observed in microglia from aged animals and exercise ameliorated these effects, while it also increased the phagocytic capacity of cells. The senescent markers, β-galactosidase and p16INK4A, were increased in microglia from sedentary aged mice, and expression of these markers was significantly decreased by exercise. The data demonstrate that the exercise-related improved cognition is orchestrated by a normalization of the metabolic profile and functionality of microglia.

Published
2020
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