Antigen presentation between T cells drives Th17 polarization under conditions of limiting antigen.
Antigen presentation between T cells drives Th17 polarization under conditions of limiting antigen.
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DOI:
10.1016/j.celrep.2021.108861
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发表时间:
2021-03-16
期刊:
影响因子:
8.8
通讯作者:
Alarcón B
中科院分区:
文献类型:
--
作者:
Boccasavia VL;Bovolenta ER;Villanueva A;Borroto A;Oeste CL;van Santen HM;Prieto C;Alonso-López D;Diaz-Muñoz MD;Batista FD;Alarcón B
T cells form immunological synapses with professional antigen-presenting cells (APCs) resulting in T cell activation and the acquisition of peptide antigen-MHC (pMHC) complexes from the plasma membrane of the APC. They thus become APCs themselves. We investigate the functional outcome of T-T cell antigen presentation by CD4 T cells and find that the antigen-presenting T cells (Tpres) predominantly differentiate into regulatory T cells (Treg), whereas T cells that have been stimulated by Tpres cells predominantly differentiate into Th17 pro-inflammatory cells. Using mice deficient in pMHC uptake by T cells, we show that T-T antigen presentation is important for the development of experimental autoimmune encephalitis and Th17 cell differentiation in vivo. By varying the professional APC:T cell ratio, we can modulate Treg versus Th17 differentiation in vitro and in vivo, suggesting that T-T antigen presentation underlies proinflammatory responses in conditions of antigen scarcity. CD4 T cells take up antigen/MHC complexes and present them to cognate T cells After T-T cell antigen presentation, responding T cells differentiate into Th17 T-T antigen presentation underlies Th17 generation in autoimmunity and viral infection Scarcity of antigen leads to Th17 differentiation, whereas abundance leads to Treg Boccasavia et al. show that T cells acquire antigen/MHC from professional antigen-presenting cells and convert themselves into presenting cells for other T cells of the same antigen specificity. Such T-T antigen presentation results in differentiation of the responding T cells into Th17 that mediate autoimmunity and responses to viral infections
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影响因子:
--
作者:
Cunningham EC;Sharland AF;Bishop GA
通讯作者:
Bishop GA
DOI:
10.1084/jem.191.7.1137
发表时间:
2000-04-03
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Hwang I;Huang JF;Kishimoto H;Brunmark A;Peterson PA;Jackson MR;Surh CD;Cai Z;Sprent J
通讯作者:
Sprent J
影响因子:
32.4
作者:
Martínez-Martín N;Fernández-Arenas E;Cemerski S;Delgado P;Turner M;Heuser J;Irvine DJ;Huang B;Bustelo XR;Shaw A;Alarcón B
通讯作者:
Alarcón B
影响因子:
4.4
作者:
Hudrisier, D;Riond, J;Joly, E
通讯作者:
Joly, E
影响因子:
7.3
作者:
Dhainaut M;Moser M
通讯作者:
Moser M