Toll-like receptor 2 signaling in CD4+ T lymphocytes promotes T helper 17 responses and regulates the pathogenesis of autoimmune disease (Immunity, 2010, 32:692-702)

報告日期: 2010/10/19
報告時間: 15:10/16:00
報告學生: 彭佳琇(英文報告)
講評老師: 凌 斌

Full text:

Toll-like Receptor 2 Signaling in CD4+ T Lymphocytes Promotes T Helper 17 Responses and Regulates the Pathogenesis of Autoimmune Disease


Jseph M. Reynolds, Bhanu P. Pappu, Juan Peng, Gustavo J. Martinez, Yongliang Zhang, Yeonseok Chung, Li Ma, Xuexian O. Yang, Roza I. Nurieva, Qiang Tian, and Chen Dongo

Immunity. 2010 May 28;32(5):692-702.


Speaker: Jia-Shiou Peng

Commentator: Dr. Pin Ling

Date: 2010/10/19 15:10-16:00

Place: Room 602



Innate immune responses are regulated by Toll-like receptors (TLRs), which are mainly expressed on antigen-presenting cells (APCs), such as macrophages or dendritic cells, recognize bacterial and microbial products, and signal the production of proinflammatory cytokines. TLR2 and TLR4 activate the innate function of gd T cells, resulting in the production of the cytokines interleukin-17 (IL-17).  IL-17 plays a major role in pathogenesis of experimental autoimmune encephalomyelitis (EAE).  In this study, the authors investigated the direct role of TLR2 in the generation and function of Th17 cells in vitro and in vivo. At first, to analyze TLR expression in T cell subsets and Th subsets. They found that TLR1, -2, and -6 mRNAs were expressed to the highest degree in Th17 cells. Besides, TLR2 activation in CD4+ T cells in vitro could modulate Th17 differentiation and this effect was TLR2-specific. TLR2 activation induces Th17-related genes, including IL-17, IL-17F, IL-21, CCR6, which revealed an enhancement of RORg, RORa, and IRF-4 expression. Moreover, TLR2 and IL-23 are critical in proliferation or maintenance of IL-17-producing gd T cells. Subsequently, the authors evaluated the direct role of TLR2 signaling in the regulation of Th17 cells in vivo. They found that TLR2 deficiency in CD4+ T cells decrease IL-17 production that impiars pathogenesis of EAE. In conclusion, this study demonstrates that TLR2 directly regulates Th17 responses and Th17-mediated autoimmune disease.



1.     Martin, B., Hirota, K., Cua, D.J., Stockinger, B., and Veldhoen, M. (2009). Interleukin-17-producing gammadelta T cells selectively expand in response to pathogen products and environmental signals. Immunity 31, 321–330.