@article{698d6a8ad631410b91a5cdce83d304b5,
title = "The Innate Immune Sensor NLRC3 Acts as a Rheostat that Fine-Tunes T Cell Responses in Infection and Autoimmunity",
abstract = " NLRC3 limits inflammatory signaling in myeloid cells, but its role in T cells has been unclear. Uchimura et al. reveal that T cell expression of Nlrc3 restricts autoimmune and virus-specific CD4 + T cell responses by attenuating T cell signaling and metabolic pathways in CD4 + T cells. ",
keywords = "autoimmunity, CD4 T cell response, EAE, inflammatory pathways, LCMV infection, NLRC3, NOD-like receptors, T cell receptor signaling",
author = "Toru Uchimura and Yoshitaka Oyama and Meng Deng and Haitao Guo and Wilson, {Justin E.} and Elena Rampanelli and Cook, {Kevin D.} and Ichiro Misumi and Xianming Tan and Liang Chen and Brandon Johnson and Jason Tam and Chou, {Wei Chun} and Brickey, {W. June} and Alex Petrucelli and Whitmire, {Jason K.} and Ting, {Jenny P.Y.}",
note = "Funding Information: We thank the Flow Cytometry Core Facility at University of North Carolina at Chapel Hill for providing core and technical support. This work was supported by NIH grants AI029564 , CA156330 , DK094779 , and CA10068 (the last to the National Multiple Sclerosis Society) to J.P.-Y.T. and U19AI109965 to J.P.-Y.T. and J.K.W. T.U. was supported by the Japanese vaccine research fellowship ( Japan Foundation for Pediatric Research ). We thank Dr. Shumpei Yokota and Dr.Shuichi Ito for editing the manuscript and Dr. Vijay Kuchroo for generously providing the 2D2 transgenic strain. Publisher Copyright: {\textcopyright} 2018 Elsevier Inc.",
year = "2018",
month = dec,
day = "18",
doi = "10.1016/j.immuni.2018.10.008",
language = "English (US)",
volume = "49",
pages = "1049--1061.e6",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "6",
}