γδ T Cells Enhance Autoimmunity by Restraining Regulatory T Cell Responses via an Interleukin-23-Dependent Mechanism

Petermann F, Rothhammer V, Claussen MC, Haas JD, Blanco LR, Heink S, Prinz I, Hemmer B, Kuchroo VK, Oukka M, Korn T (2010)


Publication Type: Journal article

Publication year: 2010

Journal

Book Volume: 33

Pages Range: 351-363

Journal Issue: 3

DOI: 10.1016/j.immuni.2010.08.013

Abstract

Mice that lack interleukin-23 (IL-23) are resistant to T cell-mediated autoimmunity. Although IL-23 is a maturation factor for T helper 17 (Th17) cells, a subset of γδ T cells expresses the IL-23 receptor (IL-23R) constitutively. Using IL-23R reporter mice, we showed that γδ T cells were the first cells to respond to IL-23 during experimental autoimmune encephalomyelitis (EAE). Although γδ T cells produced Th17 cell-associated cytokines in response to IL-23, their major function was to prevent the development of regulatory T (Treg) cell responses. IL-23-activated γδ T cells rendered αβ effector T cells refractory to the suppressive activity of Treg cells and also prevented the conversion of conventional T cells into Foxp3+ Treg cells in vivo. Thus, IL-23, which by itself has no direct effect on Treg cells, is able to disarm Treg cell responses and promote antigen-specific effector T cell responses via activating γδ T cells. © 2010 Elsevier Inc.

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APA:

Petermann, F., Rothhammer, V., Claussen, M.C., Haas, J.D., Blanco, L.R., Heink, S.,... Korn, T. (2010). γδ T Cells Enhance Autoimmunity by Restraining Regulatory T Cell Responses via an Interleukin-23-Dependent Mechanism. Immunity, 33(3), 351-363. https://doi.org/10.1016/j.immuni.2010.08.013

MLA:

Petermann, Franziska, et al. "γδ T Cells Enhance Autoimmunity by Restraining Regulatory T Cell Responses via an Interleukin-23-Dependent Mechanism." Immunity 33.3 (2010): 351-363.

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