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Başlık: Unique and shared signaling pathways cooperate to regulate the differentiation of human CD4(+) T cells into distinct effector subsets
Yazarlar: Ma, Cindy S.
Wong, Natalie
Rao, Geetha
Nguyen, Akira
Avery, Danielle T.
Payne, Kathryn
Torpy, James
O'Young, Patrick
Deenick, Elissa
Bustamante, Jacinta
Puel, Anne
Okada, Satoshi
Kobayashi, Masao
Martinez-Barricarte, Ruben
Elliott, Michael
El Baghdadi, Jamila
Minegishi, Yoshiyuki
Bousfiha, Aziz
Robertson, Nic
Hambleton, Sophie
Arkwright, Peter D.
French, Martyn
Blincoe, Annaliesse K.
Hsu, Peter
Campbell, Dianne E.
Stormon, Michael O.
Wong, Melanie
Adelstein, Stephen
Fulcher, David A.
Cook, Matthew C.
Stepensky, Polina
Boztuğ, Kaan
Beier, Rita
İkincioğulları, Aydan
Ziegler, John B.
Gray, Paul
Picard, Capucine
Boisson-Dupuis, Stephanie
Tri Giang, Phan
Grimbacher, Bodo
Warnatz, Klaus
Holland, Steven M.
Uzel, Gülbü
Casanova, Jean-Laurent
Tangye, Stuart G.
Uludağ Üniversitesi/Tıp Fakültesi/Çocuk Sağlığı ve Hastalıkları Anabilim Dalı.
Kılıç, Sara Şebnem
AAH-1658-2021
34975059200
Anahtar kelimeler: Hyper-ige syndrome
Chronic mucocutaneous candidiasis
Follicular-helper-cells
Common variable immunodeficiency
Essential modulator mutation
Antibody-responses
Ectodermal dysplasia
IL-10 production
Icos deficiency
BCL6 expression
Yayın Tarihi: 25-Tem-2016
Yayıncı: Rockefeller University Press
Atıf: Ma, C. S. vd. (2016). "Unique and shared signaling pathways cooperate to regulate the differentiation of human CD4(+) T cells into distinct effector subsets". Journal of Experimental Medicine, 213(8), 1589-1608.
Özet: Naive CD4(+) T cells differentiate into specific effector subsets-Th1, Th2, Th17, and T follicular helper (Tfh)-that provide immunity against pathogen infection. The signaling pathways involved in generating these effector cells are partially known. However, the effects of mutations underlying human primary immunodeficiencies on these processes, and how they compromise specific immune responses, remain unresolved. By studying individuals with mutations in key signaling pathways, we identified nonredundant pathways regulating human CD4(+) T cell differentiation in vitro. IL12R beta 1/TYK2 and IFN-gamma R/STAT1 function in a feed-forward loop to induce Th1 cells, whereas IL-21/IL-21R/STAT3 signaling is required for Th17, Tfh, and IL-10-secreting cells. IL12R beta 1/TYK2 and NEMO are also required for Th17 induction. Strikingly, gain-of-function STAT1 mutations recapitulated the impact of dominant-negative STAT3 mutations on Tfh and Th17 cells, revealing a putative inhibitory effect of hypermorphic STAT1 over STAT3. These findings provide mechanistic insight into the requirements for human T cell effector function, and explain clinical manifestations of these immunodeficient conditions. Furthermore, they identify molecules that could be targeted to modulate CD4(+) T cell effector function in the settings of infection, vaccination, or immune dysregulation.
URI: https://doi.org/10.1084/jem.20151467
https://rupress.org/jem/article/213/8/1589/42083/Unique-and-shared-signaling-pathways-cooperate-to
http://hdl.handle.net/11452/28838
ISSN: 0022-1007
1540-9538
Koleksiyonlarda Görünür:PubMed
Scopus
Web of Science

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