@article{d29daafc21154926934701bbd000b5cd,
title = "Toll-like receptor 2 signaling in CD4+ T lymphocytes promotes T helper 17 responses and regulates the pathogenesis of autoimmune disease",
abstract = "Toll-like receptors (TLRs) have previously been shown to play critical roles in the activation of innate immunity. Here, we describe that T cell expression of TLR2 regulates T helper 17 (Th17) cell responses. Stimulation with TLR2 agonists promoted Th17 differentiation in vitro and led to more robust proliferation and Th17 cytokine production. Using the experimental autoimmune encephalomyelitis (EAE) model, we found that TLR2 regulated Th17 cell-mediated autoimmunity in vivo and that loss of TLR2 in CD4+ T cells dramatically ameliorated EAE. This study thus reveals a critical role of a TLR in the direct regulation of adaptive immune response and pathogenesis of autoimmune diseases.",
keywords = "Cellimmuno, Molimmuno",
author = "Reynolds, {Joseph M.} and Pappu, {Bhanu P.} and Juan Peng and Martinez, {Gustavo J.} and Yongliang Zhang and Yeonseok Chung and Li Ma and Yang, {Xuexian O.} and Nurieva, {Roza I.} and Qiang Tian and Chen Dong",
note = "Funding Information: We thank the flow cytometry core facility at the M.D. Anderson Cancer Center and the entire Dong lab for their help and suggestions. This work is supported by research grants from the National Institutes of Health (NIH to C.D. and R.I.N.). J.M.R. is a recipient of a T32 training grant from the National Cancer Institute (NCI). B.P.P. received an Odyssey Fellowship from the M.D. Anderson Cancer Center. G.J.M. was a Schissler Foundation M.D. Anderson Cancer Center Fellow in cancer research. R.I.N. was a recipient of a Scientist Development Grant from the American Heart Association (AHA). C.D. is a Leukemia & Lymphoma Society Scholar and a Trust Fellow of the M.D. Anderson Cancer Center. ",
year = "2010",
month = may,
doi = "10.1016/j.immuni.2010.04.010",
language = "English (US)",
volume = "32",
pages = "692--702",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "5",
}