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Your search keyword '"Moir, Susan L."' showing total 4 results
Start Over Author "Moir, Susan L." Publication Type Academic Journals
4 results on '"Moir, Susan L."'

1. Constitutively active Lyn kinase causes a cutaneous small vessel vasculitis and liver fibrosis syndrome

Author

de Jesus, Adriana A., Chen, Guibin, Yang, Dan, Brdicka, Tomas, Ruth, Natasha M., Bennin, David, Cebecauerova, Dita, Malcova, Hana, Freeman, Helen, Martin, Neil, Svojgr, Karel, Passo, Murray H., Bhuyan, Farzana, Alehashemi, Sara, Rastegar, Andre T., Uss, Katsiaryna, Kardava, Lela, Marrero, Bernadette, Duric, Iris, Omoyinmi, Ebun, Peldova, Petra, Lee, Chyi-Chia Richard, Kleiner, David E., Hadigan, Colleen M., Hewitt, Stephen M., Pittaluga, Stefania, Carmona-Rivera, Carmelo, Calvo, Katherine R., Shah, Nirali, Balascakova, Miroslava, Fink, Danielle L., Kotalova, Radana, Parackova, Zuzana, Peterkova, Lucie, Kuzilkova, Daniela, Campr, Vit, Sramkova, Lucie, Biancotto, Angelique, Brooks, Stephen R., Manes, Cameron, Meffre, Eric, Harper, Rebecca L., Kuehn, Hyesun, Kaplan, Mariana J., Brogan, Paul, Rosenzweig, Sergio D., Merchant, Melinda, Deng, Zuoming, Huttenlocher, Anna, Moir, Susan L., Kuhns, Douglas B., Boehm, Manfred, Skvarova Kramarzova, Karolina, and Goldbach-Mansky, Raphaela

Published
2023
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2. Early-Onset Stroke and Vasculopathy Associated with Mutations in ADA2

Author

Zhou, Qing, Yang, Dan, Ombrello, Amanda K., Zavialov, Andrey V., Toro, Camilo, Zavialov, Anton V., Stone, Deborah L., Chae, Jae Jin, Rosenzweig, Sergio D., Bishop, Kevin, Barron, Karyl S., Kuehn, Hye Sun, Hoffmann, Patrycja, Negro, Alejandra, Tsai, Wanxia L., Cowen, Edward W., Pei, Wuhong, Milner, Joshua D., Silvin, Christopher, Heller, Theo, Chin, David T., Patronas, Nicholas J., Barber, John S., Lee, Chyi-Chia R., Wood, Geryl M., Ling, Alexander, Kelly, Susan J., Kleiner, David E., Mullikin, James C., Ganson, Nancy J., Kong, Heidi H., Hambleton, Sophie, Candotti, Fabio, Quezado, Martha M., Calvo, Katherine R., Alao, Hawwa, Barham, Beverly K., Jones, Anne, Meschia, James F., Worrall, Bradford B., Kasner, Scott E., Rich, Stephen S., Goldbach-Mansky, Raphaela, Abinun, Mario, Chalom, Elizabeth, Gotte, Alisa C., Punaro, Marilynn, Pascual, Virginia, Verbsky, James W., Torgerson, Troy R., Singer, Nora G., Gershon, Timothy R., Ozen, Seza, Karadag, Omer, Fleisher, Thomas A., Remmers, Elaine F., Burgess, Shawn M., Moir, Susan L., Gadina, Massimo, Sood, Raman, Hershfield, Michael S., Boehm, Manfred, Kastner, Daniel L., and Aksentijevich, Ivona

Published
2014
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3. SIV infection of rhesus macaques results in dysfunctional T- and B-cell responses to neo and recall Leishmania major vaccination.

Author

Klatt, Nichole R., Vinton, Carol L., Lynch, Rebecca M., Canary, Lauren A., Ho, Jason, Darrah, Patricia A., Estes, Jacob D., Seder, Robert A., Moir, Susan L., and Brenchley, Jason M.

Subjects
*HIV infections, *T cells, *B cells, *LEISHMANIA, *IMMUNE response, *ANTIGENS
Abstract

HIV infection is characterized by immune system dysregulation, including depletion of CD4+ T cells, immune activation, and abnormal B- and T-cell responses. However, the immunologic mechanisms underlying lymphocytic dysfunctionality and whether it is restricted to immune responses against neo antigens, recall antigens, or both is unclear. Here, we immunized SIV-infected and uninfected rhesus macaques to induce immune responses against neo and recall antigens using a Leishmania major polyprotein (MML) vaccine given with poly-ICLC adjuvant. We found that vaccinated SIVuninfected animals induced high frequencies of polyfunctional MML-specific CD4+ T cells. However, in SIV-infected animals, CD4+ T-cell functionality decreased after both neo (P = .0025) and recall (P = .0080) MML vaccination. Furthermore, after SIV infection, the frequency of MML-specific antibody-secreting classic memory B cells was decreased compared with vaccinated, SIV-uninfected animals. Specifically, antibody-secreting classic memory B cells that produced IgA in response to either neo (P = .0221) or recall (P = .0356) MML vaccinations were decreased. Furthermore, we found that T-follicular helper cells, which are essential for priming B cells, are preferentially infected with SIV. These data indicate that SIV infection results in dysfunctional T-cell responses to neo and recall vaccinations, and direct SIV infection of T-follicular helper cells, both of which probably contribute to deficient B-cell responses and, presumably, susceptibility to certain opportunistic infections. [ABSTRACT FROM AUTHOR]

Published
2011
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4. HIV vaccines induce CD8 + T cells with low antigen receptor sensitivity.

Author

Migueles SA, Nettere DM, Gavil NV, Wang LT, Toulmin SA, Kelly EP, Ward AJ, Lin S, Thompson SA, Peterson BA, Abdeen CS, Sclafani CR, Pryal PF, Leach BG, Ludwig AK, Rogan DC, Przygonska PA, Cattani A, Imamichi H, Sachs A, Cafri G, Huang NN, Patamawenu A, Liang CJ, Hallahan CW, Kambach DM, Han EX, Coupet T, Chen J, Moir SL, Chun TW, Coates EE, Ledgerwood J, Schmidt J, Taillandier-Coindard M, Michaux J, Pak H, Bassani-Sternberg M, Frahm N, McElrath MJ, and Connors M

Subjects
Humans, Clone Cells, Receptors, Antigen, T-Cell metabolism, AIDS Vaccines immunology, HIV Infections prevention & control, Cytotoxicity, Immunologic, T-Lymphocytes, Cytotoxic immunology, Cell Degranulation immunology
Abstract

Current HIV vaccines designed to stimulate CD8 + T cells have failed to induce immunologic control upon infection. The functions of vaccine-induced HIV-specific CD8 + T cells were investigated here in detail. Cytotoxic capacity was significantly lower than in HIV controllers and was not a consequence of low frequency or unaccumulated functional cytotoxic proteins. Low cytotoxic capacity was attributable to impaired degranulation in response to the low antigen levels present on HIV-infected targets. The vaccine-induced T cell receptor (TCR) repertoire was polyclonal and transduction of these TCRs conferred the same reduced functions. These results define a mechanism accounting for poor antiviral activity induced by these vaccines and suggest that an effective CD8 + T cell response may require a vaccination strategy that drives further TCR clonal selection.

Published
2023
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