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2,256 results on '"Colonna, Marco"'

1. Neuroinflammation in Alzheimer disease

Author

Heneka, Michael T., van der Flier, Wiesje M., Jessen, Frank, Hoozemanns, Jeroen, Thal, Dietmar Rudolf, Boche, Delphine, Brosseron, Frederic, Teunissen, Charlotte, Zetterberg, Henrik, Jacobs, Andreas H., Edison, Paul, Ramirez, Alfredo, Cruchaga, Carlos, Lambert, Jean-Charles, Laza, Agustin Ruiz, Sanchez-Mut, Jose Vicente, Fischer, Andre, Castro-Gomez, Sergio, Stein, Thor D., Kleineidam, Luca, Wagner, Michael, Neher, Jonas J., Cunningham, Colm, Singhrao, Sim K., Prinz, Marco, Glass, Christopher K., Schlachetzki, Johannes C. M., Butovsky, Oleg, Kleemann, Kilian, De Jaeger, Philip L., Scheiblich, Hannah, Brown, Guy C., Landreth, Gary, Moutinho, Miguel, Grutzendler, Jaime, Gomez-Nicola, Diego, McManus, Róisín M., Andreasson, Katrin, Ising, Christina, Karabag, Deniz, Baker, Darren J., Liddelow, Shane A., Verkhratsky, Alexei, Tansey, Malu, Monsonego, Alon, Aigner, Ludwig, Dorothée, Guillaume, Nave, Klaus-Armin, Simons, Mikael, Constantin, Gabriela, Rosenzweig, Neta, Pascual, Alberto, Petzold, Gabor C., Kipnis, Jonathan, Venegas, Carmen, Colonna, Marco, Walter, Jochen, Tenner, Andrea J., O’Banion, M. Kerry, Steinert, Joern R., Feinstein, Douglas L., Sastre, Magdalena, Bhaskar, Kiran, Hong, Soyon, Schafer, Dorothy P., Golde, Todd, Ransohoff, Richard M., Morgan, David, Breitner, John, Mancuso, Renzo, and Riechers, Sean-Patrick

Published
2024
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2. Implementation and validation of single-cell genomics experiments in neuroscience

Author

Colonna, Marco, Konopka, Genevieve, Liddelow, Shane A., Nowakowski, Tomasz, Awatramani, Rajeshwar, Bateup, Helen S., Cadwell, Cathryn R., Caglayan, Emre, Chen, Jerry L., Gillis, Jesse, Kampmann, Martin, Krienen, Fenna, Marsh, Samuel E., Monje, Michelle, O’Dea, Michael R., Patani, Rickie, Pollen, Alex A., Quintana, Francisco J., Scavuzzo, Marissa, Schmitz, Matthew, Sloan, Steven A., Tesar, Paul J., Tollkuhn, Jessica, Tosches, Maria Antonietta, Urbanek, Madeleine E., Werner, Jonathan M., Bayraktar, Omer A., Gokce, Ozgun, and Habib, Naomi

Published
2024
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3. High-dimensional single-cell analysis of human natural killer cell heterogeneity.

Author

Rebuffet, Lucas, Melsen, Janine, Escalière, Bertrand, Basurto-Lozada, Daniela, Bhandoola, Avinash, Björkström, Niklas, Bryceson, Yenan, Castriconi, Roberta, Cichocki, Frank, Colonna, Marco, Davis, Daniel, Diefenbach, Andreas, Ding, Yi, Haniffa, Muzlifah, Horowitz, Amir, Lanier, Lewis, Malmberg, Karl-Johan, Miller, Jeffrey, Moretta, Lorenzo, Narni-Mancinelli, Emilie, ONeill, Luke, Romagnani, Chiara, Ryan, Dylan, Sivori, Simona, Sun, Dan, Vagne, Constance, and Vivier, Eric

Subjects
Humans, Single-Cell Analysis, Killer Cells, Natural, Transcriptome, Neoplasms, Lymphocyte Subsets, Palatine Tonsil, Gene Expression Profiling, Lung, Cytokines
Abstract

Natural killer (NK) cells are innate lymphoid cells (ILCs) contributing to immune responses to microbes and tumors. Historically, their classification hinged on a limited array of surface protein markers. Here, we used single-cell RNA sequencing (scRNA-seq) and cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) to dissect the heterogeneity of NK cells. We identified three prominent NK cell subsets in healthy human blood: NK1, NK2 and NK3, further differentiated into six distinct subgroups. Our findings delineate the molecular characteristics, key transcription factors, biological functions, metabolic traits and cytokine responses of each subgroup. These data also suggest two separate ontogenetic origins for NK cells, leading to divergent transcriptional trajectories. Furthermore, we analyzed the distribution of NK cell subsets in the lung, tonsils and intraepithelial lymphocytes isolated from healthy individuals and in 22 tumor types. This standardized terminology aims at fostering clarity and consistency in future research, thereby improving cross-study comparisons.

Published
2024

4. Amplification of autoimmune organ damage by NKp46-activated ILC1s

Author

Biniaris-Georgallis, Stylianos-Iason, Aschman, Tom, Stergioula, Katerina, Schreiber, Frauke, Jafari, Vajiheh, Taranko, Anna, Karmalkar, Tejal, Kasapi, Ana, Lenac Rovis, Tihana, Jelencic, Vedrana, Bejarano, David A., Fabry, Lea, Papacharalampous, Michail, Mattiola, Irene, Molgora, Martina, Hou, Jinchao, Hublitz, Karolin W., Heinrich, Frederik, Guerra, Gabriela Maria, Durek, Pawel, Patone, Giannino, Lindberg, Eric L., Maatz, Henrike, Hölsken, Oliver, Krönke, Gerhard, Mortha, Arthur, Voll, Reinhard E., Clarke, Alexander J., Hauser, Anja E., Colonna, Marco, Thurley, Kevin, Schlitzer, Andreas, Schneider, Christoph, Stamatiades, Efstathios G., Mashreghi, Mir-Farzin, Jonjic, Stipan, Hübner, Norbert, Diefenbach, Andreas, Kanda, Masatoshi, and Triantafyllopoulou, Antigoni

Published
2024
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5. Inositol phosphatase INPP4B sustains ILC1s and intratumoral NK cells through an AKT-driven pathway.

Author

Peng, Vincent, Trsan, Tihana, Sudan, Raki, Bhattarai, Bishan, Cortez, Victor, Molgora, Martina, Vacher, Jean, and Colonna, Marco

Subjects
Proto-Oncogene Proteins c-akt, Immunity, Innate, Killer Cells, Natural, Homeostasis
Abstract

Innate lymphoid cells (ILCs) are a heterogeneous population of lymphocytes that coordinate early immune responses and maintain tissue homeostasis. Type 1 innate immune responses are mediated by natural killer (NK) cells and group 1 ILCs (ILC1s). Despite their shared features, NK cells and ILC1s display profound differences among various tissue microenvironments. Here, we identify the inositol polyphosphatase INPP4B as a hallmark feature of tissue-resident ILC1s and intratumoral NK cells using an scRNA-seq atlas of tissue-associated and circulating NK/ILC1s. Conditional deletion of Inpp4b in ILC1s and NK cells reveals that it is necessary for the homeostasis of tissue-resident ILC1s but not circulating NK cells at steady-state. Inpp4b-deficient cells display increased rates of apoptosis and reduced activation of the prosurvival molecule AKT. Furthermore, expression of Inpp4b by NK/ILC1s is necessary for their presence in the intratumoral environment, and lack of Inpp4b impairs antitumor immunity. These findings highlight INPP4B as a novel regulator of tissue residency and antitumor function in ILC1s and NK cells.

Published
2024

6. Neoantigen-specific cytotoxic Tr1 CD4 T cells suppress cancer immunotherapy

Author

Sultan, Hussein, Takeuchi, Yoshiko, Ward, Jeffrey P., Sharma, Naveen, Liu, Tian-Tian, Sukhov, Vladimir, Firulyova, Maria, Song, Yuang, Ameh, Samuel, Brioschi, Simone, Khantakova, Darya, Arthur, Cora D., White, J. Michael, Kohlmiller, Heather, Salazar, Andres M., Burns, Robert, Costa, Helio A., Moynihan, Kelly D., Yeung, Yik Andy, Djuretic, Ivana, Schumacher, Ton N., Sheehan, Kathleen C. F., Colonna, Marco, Allison, James P., Murphy, Kenneth M., Artyomov, Maxim N., and Schreiber, Robert D.

Published
2024
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8. Plasmacytoid dendritic cells control homeostasis of megakaryopoiesis

Author

Gaertner, Florian, Ishikawa-Ankerhold, Hellen, Stutte, Susanne, Fu, Wenwen, Weitz, Jutta, Dueck, Anne, Nelakuditi, Bhavishya, Fumagalli, Valeria, van den Heuvel, Dominic, Belz, Larissa, Sobirova, Gulnoza, Zhang, Zhe, Titova, Anna, Navarro, Alejandro Martinez, Pekayvaz, Kami, Lorenz, Michael, von Baumgarten, Louisa, Kranich, Jan, Straub, Tobias, Popper, Bastian, Zheden, Vanessa, Kaufmann, Walter Anton, Guo, Chenglong, Piontek, Guido, von Stillfried, Saskia, Boor, Peter, Colonna, Marco, Clauß, Sebastian, Schulz, Christian, Brocker, Thomas, Walzog, Barbara, Scheiermann, Christoph, Aird, William C., Nerlov, Claus, Stark, Konstantin, Petzold, Tobias, Engelhardt, Stefan, Sixt, Michael, Hauschild, Robert, Rudelius, Martina, Oostendorp, Robert A. J., Iannacone, Matteo, Heinig, Matthias, and Massberg, Steffen

Published
2024
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9. TREM2 protects from atherosclerosis by limiting necrotic core formation

Author

Piollet, Marie, Porsch, Florentina, Rizzo, Giuseppe, Kapser, Frederieke, Schulz, Dirk J. J., Kiss, Máté G., Schlepckow, Kai, Morenas-Rodriguez, Estrella, Sen, Mustafa Orkun, Gropper, Julius, Bandi, Sourish Reddy, Schäfer, Sarah, Krammer, Tobias, Leipold, Alexander M., Hoke, Matthias, Ozsvár-Kozma, Mária, Beneš, Hannah, Schillinger, Martin, Minar, Erich, Roesch, Melanie, Göderle, Laura, Hladik, Anastasiya, Knapp, Sylvia, Colonna, Marco, Martini, Rudolf, Saliba, Antoine-Emmanuel, Haass, Christian, Zernecke, Alma, Binder, Christoph J., and Cochain, Clément

Published
2024
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11. TREM2-independent microgliosis promotes tau-mediated neurodegeneration in the presence of ApoE4.

Author

Gratuze, Maud, Schlachetzki, Johannes, DOliveira Albanus, Ricardo, Jain, Nimansha, Novotny, Brenna, Brase, Logan, Rodriguez, Lea, Mansel, Clayton, Kipnis, Michal, OBrien, Sydney, Pasillas, Martina, Lee, Choonghee, Manis, Melissa, Colonna, Marco, Harari, Oscar, Glass, Christopher, Ulrich, Jason, and Holtzman, David

Subjects
Alzheimer’s disease, ApoE4, TREM2, microgliosis, tau pathology, tau-mediated neurodegeneration, Mice, Animals, Apolipoprotein E4, Alzheimer Disease, Inflammation, Microglia, Disease Models, Animal, Membrane Glycoproteins, Receptors, Immunologic
Abstract

In addition to tau and Aβ pathologies, inflammation plays an important role in Alzheimers disease (AD). Variants in APOE and TREM2 increase AD risk. ApoE4 exacerbates tau-linked neurodegeneration and inflammation in P301S tau mice and removal of microglia blocks tau-dependent neurodegeneration. Microglia adopt a heterogeneous population of transcriptomic states in response to pathology, at least some of which are dependent on TREM2. Previously, we reported that knockout (KO) of TREM2 attenuated neurodegeneration in P301S mice that express mouse Apoe. Because of the possible common pathway of ApoE and TREM2 in AD, we tested whether TREM2 KO (T2KO) would block neurodegeneration in P301S Tau mice expressing ApoE4 (TE4), similar to that observed with microglial depletion. Surprisingly, we observed exacerbated neurodegeneration and tau pathology in TE4-T2KO versus TE4 mice, despite decreased TREM2-dependent microgliosis. Our results suggest that tau pathology-dependent microgliosis, that is, TREM2-independent microgliosis, facilitates tau-mediated neurodegeneration in the presence of ApoE4.

Published
2023

12. Mucosal Single-Cell Profiling of Crohn’s-Like Disease of the Pouch Reveals Unique Pathogenesis and Therapeutic Targets

Author

Cao, Siyan, Nguyen, Khai M., Ma, Kaiming, Du, Xiaotang, Liu, Xiuli, Ulezko Antonova, Alina, Rood, Richard P., Gremida, Anas, Chen, Chien-Huan, Gutierrez, Alexandra, Rubin, Deborah C., Gregory, Martin H., Gergely, Mate, Escudero, Guadalupe Oliva, Huang, Katherine, Jaeger, Natalia, Cella, Marina, Newberry, Rodney D., Davidson, Nicholas O., Ciorba, Matthew A., Deepak, Parakkal, and Colonna, Marco

Published
2024
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14. Microglia states and nomenclature: A field at its crossroads

Author

Paolicelli, Rosa C, Sierra, Amanda, Stevens, Beth, Tremblay, Marie-Eve, Aguzzi, Adriano, Ajami, Bahareh, Amit, Ido, Audinat, Etienne, Bechmann, Ingo, Bennett, Mariko, Bennett, Frederick, Bessis, Alain, Biber, Knut, Bilbo, Staci, Blurton-Jones, Mathew, Boddeke, Erik, Brites, Dora, Brône, Bert, Brown, Guy C, Butovsky, Oleg, Carson, Monica J, Castellano, Bernardo, Colonna, Marco, Cowley, Sally A, Cunningham, Colm, Davalos, Dimitrios, De Jager, Philip L, de Strooper, Bart, Denes, Adam, Eggen, Bart JL, Eyo, Ukpong, Galea, Elena, Garel, Sonia, Ginhoux, Florent, Glass, Christopher K, Gokce, Ozgun, Gomez-Nicola, Diego, González, Berta, Gordon, Siamon, Graeber, Manuel B, Greenhalgh, Andrew D, Gressens, Pierre, Greter, Melanie, Gutmann, David H, Haass, Christian, Heneka, Michael T, Heppner, Frank L, Hong, Soyon, Hume, David A, Jung, Steffen, Kettenmann, Helmut, Kipnis, Jonathan, Koyama, Ryuta, Lemke, Greg, Lynch, Marina, Majewska, Ania, Malcangio, Marzia, Malm, Tarja, Mancuso, Renzo, Masuda, Takahiro, Matteoli, Michela, McColl, Barry W, Miron, Veronique E, Molofsky, Anna Victoria, Monje, Michelle, Mracsko, Eva, Nadjar, Agnes, Neher, Jonas J, Neniskyte, Urte, Neumann, Harald, Noda, Mami, Peng, Bo, Peri, Francesca, Perry, V Hugh, Popovich, Phillip G, Pridans, Clare, Priller, Josef, Prinz, Marco, Ragozzino, Davide, Ransohoff, Richard M, Salter, Michael W, Schaefer, Anne, Schafer, Dorothy P, Schwartz, Michal, Simons, Mikael, Smith, Cody J, Streit, Wolfgang J, Tay, Tuan Leng, Tsai, Li-Huei, Verkhratsky, Alexei, von Bernhardi, Rommy, Wake, Hiroaki, Wittamer, Valérie, Wolf, Susanne A, Wu, Long-Jun, and Wyss-Coray, Tony

Subjects
Microglia, Neurosciences, Psychology, Cognitive Sciences, Neurology & Neurosurgery
Abstract

Microglial research has advanced considerably in recent decades yet has been constrained by a rolling series of dichotomies such as "resting versus activated" and "M1 versus M2." This dualistic classification of good or bad microglia is inconsistent with the wide repertoire of microglial states and functions in development, plasticity, aging, and diseases that were elucidated in recent years. New designations continuously arising in an attempt to describe the different microglial states, notably defined using transcriptomics and proteomics, may easily lead to a misleading, although unintentional, coupling of categories and functions. To address these issues, we assembled a group of multidisciplinary experts to discuss our current understanding of microglial states as a dynamic concept and the importance of addressing microglial function. Here, we provide a conceptual framework and recommendations on the use of microglial nomenclature for researchers, reviewers, and editors, which will serve as the foundations for a future white paper.

Published
2022

17. The centrosomal protein FGFR1OP controls myosin function in murine intestinal epithelial cells

Author

Trsan, Tihana, Peng, Vincent, Krishna, Chirag, Ohara, Takahiro E., Beatty, Wandy L., Sudan, Raki, Kanai, Masahiro, Krishnamoorthy, Praveen, Rodrigues, Patrick Fernandes, Fachi, Jose L., Grajales-Reyes, Gary, Jaeger, Natalia, Fitzpatrick, James A.J., Cella, Marina, Gilfillan, Susan, Nakata, Toru, Jaiswal, Alok, Stappenbeck, Thaddeus S., Daly, Mark J., Xavier, Ramnik J., and Colonna, Marco

Published
2024
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18. TREM2 macrophages induced by human lipids drive inflammation in acne lesions

Author

Do, Tran H, Ma, Feiyang, Andrade, Priscila R, Teles, Rosane, de Andrade Silva, Bruno J, Hu, Chanyue, Espinoza, Alejandro, Hsu, Jer-En, Cho, Chun-Seok, Kim, Myungjin, Xi, Jingyue, Xing, Xianying, Plazyo, Olesya, Tsoi, Lam C, Cheng, Carol, Kim, Jenny, Bryson, Bryan D, O'Neill, Alan M, Colonna, Marco, Gudjonsson, Johann E, Klechevsky, Eynav, Lee, Jun Hee, Gallo, Richard L, Bloom, Barry R, Pellegrini, Matteo, and Modlin, Robert L

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Atherosclerosis, Genetics, Clinical Research, 2.1 Biological and endogenous factors, Acne Vulgaris, Humans, Inflammation, Lipids, Macrophages, Membrane Glycoproteins, Receptors, Immunologic, Squalene, Clinical sciences
Abstract

Acne affects 1 in 10 people globally, often resulting in disfigurement. The disease involves excess production of lipids, particularly squalene, increased growth of Cutibacterium acnes, and a host inflammatory response with foamy macrophages. By combining single-cell and spatial RNA sequencing as well as ultrahigh-resolution Seq-Scope analyses of early acne lesions on back skin, we identified TREM2 macrophages expressing lipid metabolism and proinflammatory gene programs in proximity to hair follicle epithelium expressing squalene epoxidase. We established that the addition of squalene induced differentiation of TREM2 macrophages in vitro, which were unable to kill C. acnes. The addition of squalene to macrophages inhibited induction of oxidative enzymes and scavenged oxygen free radicals, providing an explanation for the efficacy of topical benzoyl peroxide in the clinical treatment of acne. The present work has elucidated the mechanisms by which TREM2 macrophages and unsaturated lipids, similar to their involvement in atherosclerosis, may contribute to the pathogenesis of acne.

Published
2022

19. The IRE1[alpha]/XBP1 pathway sustains cytokine responses of group 3 innate lymphoid cells in inflammatory bowel disease

Author

Cao, Siyan, Fachi, Jose L., Ma, Kaiming, Antonova, Alina Ulezko, Wang, Qianli, Cai, Zhangying, Kaufman, Randal J., Ciorba, Matthew A., Deepak, Parakkal, and Colonna, Marco

Subjects
Diagnosis, Care and treatment, Analysis, Dosage and administration, Inositol -- Dosage and administration, Cytokines -- Analysis, Inflammatory bowel diseases -- Diagnosis -- Care and treatment, Disease susceptibility -- Analysis
Abstract

Introduction Innate lymphoid cells (ILCs) are a group of immune cells that exhibit lymphoid characteristics yet lack antigen-specific receptors found on T and B cells (1). Group 3 ILCs (ILC3s) [...], Group 3 innate lymphoid cells (ILC3s) are key players in intestinal homeostasis. ER stress is linked to inflammatory bowel disease (IBD). Here, we used cell culture, mouse models, and human specimens to determine whether ER stress in ILC3s affects IBD pathophysiology. We show that mouse intestinal ILC3s exhibited a 24-hour rhythmic expression pattern of the master ER stress response regulator inositol-requiring kinase 1[alpha]/X-box-binding protein 1 (IRE1[alpha]/XBP1). Proinflammatory cytokine IL-23 selectively stimulated IRE1[alpha]/XBP1 in mouse ILC3s through mitochondrial ROS (mtROS). IRE1[alpha]/XBP1 was activated in ILC3s from mice exposed to experimental colitis and in inflamed human IBD specimens. Mice with Ire1[alpha] deletion in ILC3s ([Ire1[alpha].sup.[DELTA]Rorc]) showed reduced expression of the ER stress response and cytokine genes including Il22 in ILC3s and were highly vulnerable to infections and colitis. Administration of IL-22 counteracted their colitis susceptibility. In human ILC3s, IRE1 inhibitors suppressed cytokine production, which was upregulated by an IRE1 activator. Moreover, the frequencies of intestinal [XBP1s.sup.+] ILC3s in patients with Crohn's disease before administration of ustekinumab, an anti-IL-12/IL- 23 antibody, positively correlated with the response to treatment. We demonstrate that a noncanonical mtROS-IRE1[alpha]/XBP1 pathway augmented cytokine production by ILC3s and identify [XBP1s.sup.+] ILC3s as a potential biomarker for predicting the response to anti-IL-23 therapies in IBD.

Published
2024
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20. Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease

Author

Moe, Alison, Rayasam, Aditya, Sauber, Garrett, Shah, Ravi K., Doherty, Ashley, Yuan, Cheng-Yin, Szabo, Aniko, Moore, Bob M., II, Colonna, Marco, Cui, Weiguo, Romero, Julian, Zamora, Anthony E., Hillard, Cecilia J., and Drobyski, William R.

Subjects
Diagnosis, Identification and classification, Physiological aspects, Complications and side effects, Models, Development and progression, Risk factors, Health aspects, Cell receptors -- Identification and classification -- Health aspects, Inflammation -- Risk factors -- Development and progression -- Models, Cannabinoids -- Physiological aspects -- Health aspects, Graft vs. host disease -- Diagnosis -- Complications and side effects -- Models, Microglia -- Health aspects, Graft versus host reaction -- Diagnosis -- Complications and side effects -- Models
Abstract

Introduction Neurological inflammation and cognitive dysfunction are increasingly recognized complications of cancer immunotherapeutic approaches such as immune checkpoint inhibitor treatment (1, 2), chimeric antigen receptor therapy (3, 4), and graft [...], Neuroinflammation is a recognized complication of immunotherapeutic approaches such as immune checkpoint inhibitor treatment, chimeric antigen receptor therapy, and graft versus host disease (GVHD) occurring after allogeneic hematopoietic stem cell transplantation. While T cells and inflammatory cytokines play a role in this process, the precise interplay between the adaptive and innate arms of the immune system that propagates inflammation in the central nervous system remains incompletely understood. Using a murine model of GVHD, we demonstrate that type 2 cannabinoid receptor (CB2R) signaling plays a critical role in the pathophysiology of neuroinflammation. In these studies, we identify that CB2R expression on microglial cells induces an activated inflammatory phenotype that potentiates the accumulation of donor-derived proinflammatory T cells, regulates chemokine gene regulatory networks, and promotes neuronal cell death. Pharmacological targeting of this receptor with a brain penetrant CB2R inverse agonist/antagonist selectively reduces neuroinflammation without deleteriously affecting systemic GVHD severity. Thus, these findings delineate a therapeutically targetable neuroinflammatory pathway and have implications for the attenuation of neurotoxicity after GVHD and potentially other T cell-based immunotherapeutic approaches.

Published
2024
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22. Targeting TREM2 signaling shows limited impact on cerebrovascular calcification

Author

Sridhar, Sucheta; https://orcid.org/0000-0003-2699-0367, Zhou, Yingyue; https://orcid.org/0000-0002-0923-1046, Ibrahim, Adiljan, Bertazzo, Sergio; https://orcid.org/0000-0003-4889-8190, Wyss, Tania; https://orcid.org/0000-0003-2641-0895, Swain, Amanda, Maheshwari, Upasana; https://orcid.org/0000-0001-7516-3099, Huang, Sheng-Fu; https://orcid.org/0000-0002-6409-5470, Colonna, Marco; https://orcid.org/0000-0001-5222-4987, Keller, Annika; https://orcid.org/0000-0003-1466-3633, Sridhar, Sucheta; https://orcid.org/0000-0003-2699-0367, Zhou, Yingyue; https://orcid.org/0000-0002-0923-1046, Ibrahim, Adiljan, Bertazzo, Sergio; https://orcid.org/0000-0003-4889-8190, Wyss, Tania; https://orcid.org/0000-0003-2641-0895, Swain, Amanda, Maheshwari, Upasana; https://orcid.org/0000-0001-7516-3099, Huang, Sheng-Fu; https://orcid.org/0000-0002-6409-5470, Colonna, Marco; https://orcid.org/0000-0001-5222-4987, and Keller, Annika; https://orcid.org/0000-0003-1466-3633

Published
2025

23. Inulin diet uncovers complex diet-microbiota-immune cell interactions remodeling the gut epithelium

Author

Corrêa, Renan Oliveira, Castro, Pollyana Ribeiro, Fachi, José Luís, Nirello, Vinícius Dias, El-Sahhar, Salma, Imada, Shinya, Pereira, Gabriel Vasconcelos, Pral, Laís Passariello, Araújo, Nathália Vitoria Pereira, Fernandes, Mariane Font, Matheus, Valquíria Aparecida, de Souza Felipe, Jaqueline, dos Santos Pereira Gomes, Arilson Bernardo, de Oliveira, Sarah, de Rezende Rodovalho, Vinícius, de Oliveira, Samantha Roberta Machado, de Assis, Helder Carvalho, Oliveira, Sergio Costa, Dos Santos Martins, Flaviano, Martens, Eric, Colonna, Marco, Varga-Weisz, Patrick, and Vinolo, Marco Aurélio Ramirez

Published
2023
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27. Time-resolved single-cell transcriptomics defines immune trajectories in glioblastoma

Author

Kirschenbaum, Daniel, Xie, Ken, Ingelfinger, Florian, Katzenelenbogen, Yonatan, Abadie, Kathleen, Look, Thomas, Sheban, Fadi, Phan, Truong San, Li, Baoguo, Zwicky, Pascale, Yofe, Ido, David, Eyal, Mazuz, Kfir, Hou, Jinchao, Chen, Yun, Shaim, Hila, Shanley, Mayra, Becker, Soeren, Qian, Jiawen, Colonna, Marco, Ginhoux, Florent, Rezvani, Katayoun, Theis, Fabian J., Yosef, Nir, Weiss, Tobias, Weiner, Assaf, and Amit, Ido

Published
2024
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28. TREM2 macrophages drive NK cell paucity and dysfunction in lung cancer

Author

Park, Matthew D., Reyes-Torres, Ivan, LeBerichel, Jessica, Hamon, Pauline, LaMarche, Nelson M., Hegde, Samarth, Belabed, Meriem, Troncoso, Leanna, Grout, John A., Magen, Assaf, Humblin, Etienne, Nair, Achuth, Molgora, Martina, Hou, Jinchao, Newman, Jenna H., Farkas, Adam M., Leader, Andrew M., Dawson, Travis, D’Souza, Darwin, Hamel, Steven, Sanchez-Paulete, Alfonso Rodriguez, Maier, Barbara, Bhardwaj, Nina, Martin, Jerome C., Kamphorst, Alice O., Kenigsberg, Ephraim, Casanova-Acebes, Maria, Horowitz, Amir, Brown, Brian D., De Andrade, Lucas Ferrari, Colonna, Marco, Marron, Thomas U., and Merad, Miriam

Published
2023
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29. Uropathogenic Escherichia coli infection-induced epithelial trained immunity impacts urinary tract disease outcome

Author

Russell, Seongmi K., Harrison, Jessica K., Olson, Benjamin S., Lee, Hyung Joo, O’Brien, Valerie P., Xing, Xiaoyun, Livny, Jonathan, Yu, Lu, Roberson, Elisha D. O., Bomjan, Rajdeep, Fan, Changxu, Sha, Marina, Estfanous, Shady, Amer, Amal O., Colonna, Marco, Stappenbeck, Thaddeus S., Wang, Ting, Hannan, Thomas J., and Hultgren, Scott J.

Published
2023
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32. ImmGen at 15

Author

Aguilar, Stephanie Vargas, Aguilar, Oscar, Allan, Rhys, Amir, El Ad David, Angeli, Veronique, Artyomov, Maxim N, Asinovski, Natasha, Astarita, Jilian, Austen, K Frank, Bajpai, Geetika, Barrett, Nora, Baysoy, Alev, Benoist, Christophe, Bellemare-Pelletier, Angelique, Berg, Brad, Best, Adam, Bezman, Natalie, Blair, David, Blander, Julie M, Bogunovic, Milena, Brennan, Patrick, Brenner, Michael, Brown, Brian, Buechler, Matthew, Buenrostro, Jason, Casanova, Maria Acebes, Choi, Kyunghee, Chow, Andrew, Chudnovskiy, Aleksey, Cipoletta, Daniela, Cohen, Nadia, Collins, James J, Colonna, Marco, Cook, Alison, Costello, James, Cremasco, Viviana, Crowl, Ty, Crozat, Karine, Cruse, Richard, D'Angelo, June, Dalod, Marc, Davis, Scott, Demiralp, Cagatay, Deng, Tianda, Desai, Jigar V, Desland, Fiona, Dhainaut, Maxime, Ding, Jiarui, Doedens, Andrew, Dominguez, Claudia, Doran, Graeme, Dress, Regine, Dustin, Michael, Dwyer, Daniel, Dzhagalov, Ivan, Elpek, Kutlu, Ergun, Ayla, Ericson, Jeff, Esomonu, Eunice, Fairfax, Keke, Fletcher, Anne, Frascoli, Michela, Fuchs, Anja, Gainullina, Anastasiia, Gal-Oz, Shani, Gallagher, Michael, Gautier, Emmanuel, Gazit, Roi, Gibbings, Sophie, Giraud, Matthieu, Ginhoux, Florent, Goldrath, Ananda, Gotthardt, Dagmar, Gray, Daniel, Greter, Melanie, Grieshaber-Bouyer, Ricardo, Guilliams, Martin, Haidermota, Sara, Hardy, Randy, Hashimoto, Daigo, Helft, Julie, Hendricks, Deborah, Heng, Tracy, Hill, Jonathan, Hyatt, Gordon, Idoyaga, Juliana, Jakubzick, Claudia, Jarjoura, Jessica, Jepson, Daniel, Jia, Baosen, Jianu, Radu, Johanson, Tim, Jordan, Stefan, Jojic, Vladimir, Kamimura, Yosuke, Kana, Veronica, Kang, Joonsoo, Kapoor, Varun, and Kenigsberg, Ephriam

Subjects
Animals, Gene Expression Regulation, Gene Regulatory Networks, Genomics, History, 21st Century, Immune System, Immunologic Techniques, Mice, Immunological Genome Project, Immunology
Published
2020

33. A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

Author

Brioschi, Simone, Belk, Julia A., Peng, Vincent, Molgora, Martina, Rodrigues, Patrick Fernandes, Nguyen, Khai M., Wang, Shoutang, Du, Siling, Wang, Wei-Le, Grajales-Reyes, Gary E., Ponce, Jennifer M., Yuede, Carla M., Li, Qingyun, Baer, John M., DeNardo, David G., Gilfillan, Susan, Cella, Marina, Satpathy, Ansuman T., and Colonna, Marco

Published
2023
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38. Innate Lymphoid Cells and Inflammatory Bowel Disease

Author

Peng, Vincent, Jaeger, Natalia, Colonna, Marco, Crusio, Wim E., Series Editor, Dong, Haidong, Series Editor, Radeke, Heinfried H., Series Editor, Rezaei, Nima, Series Editor, Steinlein, Ortrud, Series Editor, Xiao, Junjie, Series Editor, and Sun, Xiao-Hong, editor

Published
2022
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39. Overview: Themes in Innate Lymphoid Cell Biology

Author

Colonna, Marco, Crusio, Wim E., Series Editor, Dong, Haidong, Series Editor, Radeke, Heinfried H., Series Editor, Rezaei, Nima, Series Editor, Steinlein, Ortrud, Series Editor, Xiao, Junjie, Series Editor, and Sun, Xiao-Hong, editor

Published
2022
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41. TREM2 drives microglia response to amyloid-β via SYK-dependent and -independent pathways

Author

Wang, Shoutang, Sudan, Raki, Peng, Vincent, Zhou, Yingyue, Du, Siling, Yuede, Carla M., Lei, Tingting, Hou, Jinchao, Cai, Zhangying, Cella, Marina, Nguyen, Khai, Poliani, Pietro L., Beatty, Wandy L., Chen, Yun, Cao, Siyan, Lin, Kent, Rodrigues, Cecilia, Ellebedy, Ali H., Gilfillan, Susan, Brown, Gordon D., Holtzman, David M., Brioschi, Simone, and Colonna, Marco

Published
2022
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44. Indoleamine 2,3-dioxygenase 1 activation in mature cDC1 promotes tolerogenic education of inflammatory cDC2 via metabolic communication

Author

Gargaro, Marco, Scalisi, Giulia, Manni, Giorgia, Briseño, Carlos G., Bagadia, Prachi, Durai, Vivek, Theisen, Derek J., Kim, Sunkyung, Castelli, Marilena, Xu, Chenling A., Meyer zu Hörste, Gerd, Servillo, Giuseppe, Della Fazia, Maria A., Mencarelli, Giulia, Ricciuti, Doriana, Padiglioni, Eleonora, Giacchè, Nicola, Colliva, Carolina, Pellicciari, Roberto, Calvitti, Mario, Zelante, Teresa, Fuchs, Dietmar, Orabona, Ciriana, Boon, Louis, Bessede, Alban, Colonna, Marco, Puccetti, Paolo, Murphy, Theresa L., Murphy, Kenneth M., and Fallarino, Francesca

Published
2022
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45. Intestinal epithelium–derived IL-34 reprograms macrophages to mitigate gastrointestinal tract graft-versus-host disease.

Author

Rayasam, Aditya, Moe, Alison, Kudek, Matthew, Shah, Ravi K., Yuan, Cheng-Yin, Miller, James M., Rau, Mary, Patton, Mollie, Wanat, Karolyn, Colonna, Marco, Zamora, Anthony E., and Drobyski, William R.

Subjects
REGULATORY T cells, HEMATOPOIETIC stem cell transplantation, GRANULOCYTE-macrophage colony-stimulating factor, PATHOLOGY, GASTROINTESTINAL system
Abstract

Gastrointestinal (GI) tract graft-versus-host disease (GVHD) is a major complication after allogeneic hematopoietic stem cell transplantation and is attributable to dysregulation that occurs between the effector and regulatory arms of the immune system. Whereas regulatory T cells have a primary role in counterbalancing GVHD-induced inflammation, identifying and harnessing other pathways that promote immune tolerance remain major goals in this disease. Herein, we identified interleukin-34 (IL-34) as an intestinal epithelium–derived cytokine that was able to mitigate the severity of GVHD within the GI tract. Specifically, we observed that the absence of recipient IL-34 production exacerbated GVHD lethality, promoted intestinal epithelial cell death, and compromised barrier integrity. Mechanistically, the absence of host IL-34 skewed donor macrophages toward a proinflammatory phenotype and augmented the accumulation of pathogenic CD4+ granulocyte-macrophage colony-stimulating factor (GM-CSF)+ T cells within the colon. Conversely, the administration of recombinant IL-34 substantially reduced GVHD mortality and inflammation, which was dependent on the expression of apolipoprotein E in donor macrophages. Complementary genetic and imaging approaches in mice demonstrated that intestinal epithelial cells were the relevant source of IL-34. These results were supported by colonic biopsies from patients with GVHD, which displayed IL-34 expression in intestinal epithelial cells and apolipoprotein E in lamina propria macrophages, validating similar cellular localization in humans. These studies indicate that IL-34 acts as a tissue-intrinsic cytokine that regulates GVHD severity in the GI tract and could serve as a potential therapeutic target for amelioration of this disease. Editor's summary: Although alloreactive donor T cells are the primary driver of graft-versus-host disease (GVHD), innate immune cells can also contribute to disease pathology. The specific role of macrophages, however, is less clear. Here, Rayasam et al. used a series of genetic tools and transplant studies in mice to identify a protective role for interleukin-34 (IL-34) against gastrointestinal complications in GVHD. Detailed analysis showed that IL-34 was expressed in intestinal epithelial cells after disease onset, which led to increased apolipoprotein E expression in donor macrophages and a less inflammatory phenotype. Administration of recombinant IL-34 improved symptoms and survival in mice, suggesting that targeting IL-34 could be a potential therapeutic strategy for this disease. —Allison Williams [ABSTRACT FROM AUTHOR]

Published
2025
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46. Mechanisms and environmental factors shaping the ecosystem of brain macrophages.

Author

Penati, Silvia, Brioschi, Simone, Cai, Zhangying, Han, Claudia Z., and Colonna, Marco

Subjects
YOLK sac, EVIDENCE gaps, BRAIN physiology, NEURAL development, MICROGLIA
Abstract

Brain macrophages encompass two major populations: microglia in the parenchyma and border-associated macrophages (BAMs) in the extra-parenchymal compartments. These cells play crucial roles in maintaining brain homeostasis and immune surveillance. Microglia and BAMs are phenotypically and epigenetically distinct and exhibit highly specialized functions tailored to their environmental niches. Intriguingly, recent studies have shown that both microglia and BAMs originate from the same myeloid progenitor during yolk sac hematopoiesis, but their developmental fates diverge within the brain. Several works have partially unveiled the mechanisms orchestrating the development of microglia and BAMs in both mice and humans; however, many questions remain unanswered. Defining the molecular underpinnings controlling the transcriptional and epigenetic programs of microglia and BAMs is one of the upcoming challenges for the field. In this review, we outline current knowledge on ontogeny, phenotypic diversity, and the factors shaping the ecosystem of brain macrophages. We discuss insights garnered from human studies, highlighting similarities and differences compared to mice. Lastly, we address current research gaps and potential future directions in the field. Understanding how brain macrophages communicate with their local environment and how the tissue instructs their developmental trajectories and functional features is essential to fully comprehend brain physiology in homeostasis and disease. [ABSTRACT FROM AUTHOR]

Published
2025
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47. Species- and strain-specific microbial modulation of interferon, innate immunity, and epithelial barrier in 2D air–liquid interface respiratory epithelial cultures.

Author

Horvath, Mian, Yang, Ruoyu, Castaneda, Diana Cadena, Callender, Megan, Aiken, Elizabeth S., Voigt, Anita Y., Caldwell, Ryan, Fachi, José, Di Luccia, Blanda, Scholar, Zoe, Yu, Peter, Salner, Andrew, Colonna, Marco, Palucka, Karolina, and Oh, Julia

Subjects
COLONIZATION (Ecology), NATURAL immunity, LIFE sciences, MICROBIAL diversity, GENE expression
Abstract

Background : The microbiome regulates the respiratory epithelium's immunomodulatory functions. To explore how the microbiome's biodiversity affects microbe-epithelial interactions, we screened 58 phylogenetically diverse microbes for their transcriptomic effect on human primary bronchial air–liquid interface (ALI) cell cultures. Results: We found distinct species- and strain-level differences in host innate immunity and epithelial barrier response. Strikingly, we found that host interferon, an antiviral response, was one of the most variable host processes. This variability was not driven by microbial phylogenetic diversity, bioburden, nor by the microbe's ability to stimulate other innate immunity pathways. Conclusions: Microbial colonization differentially stimulates host gene expression with variations observed across phylogenetically diverse microbes and across different strains of the same species. Our study provides a foundation for understanding how the respiratory microbiome's biodiversity affects epithelial, and particularly antiviral, innate immunity. [ABSTRACT FROM AUTHOR]

Published
2025
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50. LIGHT-HVEM Signaling in Innate Lymphoid Cell Subsets Protects Against Enteric Bacterial Infection.

Author

Seo, Goo-Young, Shui, Jr-Wen, Takahashi, Daisuke, Song, Christina, Wang, Qingyang, Kim, Kenneth, Mikulski, Zbigniew, Chandra, Shilpi, Giles, Daniel, Zahner, Sonja, Kim, Pyeung-Hyeun, Cheroutre, Hilde, Colonna, Marco, and Kronenberg, Mitchell

Subjects
CCR6, HVEM, IFN-γ, LIGHT, Yersinia enterocolitica, ileum, infection, innate lymphoid cells, Adoptive Transfer, Adult, Animals, Cytokines, Disease Models, Animal, Enterobacteriaceae Infections, Homeodomain Proteins, Host-Pathogen Interactions, Humans, Interferon-gamma, Lymphocytes, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Neuropeptides, Protein Transport, Receptors, CCR6, Receptors, Tumor Necrosis Factor, Receptors, Tumor Necrosis Factor, Member 14, Signal Transduction, Spleen, Tumor Necrosis Factor Ligand Superfamily Member 14, Yersinia enterocolitica
Abstract

Innate lymphoid cells (ILCs) are important regulators of early infection at mucosal barriers. ILCs are divided into three groups based on expression profiles, and are activated by cytokines and neuropeptides. Yet, it remains unknown if ILCs integrate other signals in providing protection. We show that signaling through herpes virus entry mediator (HVEM), a member of the tumor necrosis factor (TNF) receptor superfamily, in ILC3 is important for host defense against oral infection with the bacterial pathogen Yersinia enterocolitica. HVEM stimulates protective interferon-γ (IFN-γ) secretion from ILCs, and mice with HVEM-deficient ILC3 exhibit reduced IFN-γ production, higher bacterial burdens and increased mortality. In addition, IFN-γ production is critical as adoptive transfer of wild-type but not IFN-γ-deficient ILC3 can restore protection to mice lacking ILCs. We identify the TNF superfamily member, LIGHT, as the ligand inducing HVEM signals in ILCs. Thus HVEM signaling mediated by LIGHT plays a critical role in regulating ILC3-derived IFN-γ production for protection following infection. VIDEO ABSTRACT.

Published
2018

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