@article{4999f3cf10944591a8bcbfdda1812e9e,
title = "Checkpoint Receptor TIGIT Expressed on Tim-1+ B Cells Regulates Tissue Inflammation",
abstract = "Tim-1, a phosphatidylserine receptor expressed on B cells, induces interleukin 10 (IL-10) production by sensing apoptotic cells. Here we show that mice with B cell-specific Tim-1 deletion develop tissue inflammation in multiple organs including spontaneous paralysis with inflammation in the central nervous system (CNS). Transcriptomic analysis demonstrates that besides IL-10, Tim-1+ B cells also differentially express a number of co-inhibitory checkpoint receptors including TIGIT. Mice with B cell-specific TIGIT deletion develop spontaneous paralysis with CNS inflammation, but with limited inflammation in other organs. Our findings suggest that Tim-1+ B cells are essential for maintaining self-tolerance and restraining tissue inflammation, and that Tim-1 signaling-dependent TIGIT expression on B cells is essential for maintaining CNS-specific tolerance. A possible critical role of aryl hydrocarbon receptor (AhR) in regulating the B cell function is discussed, as we find that AhR is among the preferentially expressed transcription factors in Tim-1+ B cells and regulates their TIGIT and IL-10 expression.",
keywords = "Autoimmunity, B cells, Spontaneous inflammatory disorders, TIGIT, Tim-1, Tissue tolerance",
author = "Sheng Xiao and Lloyd Bod and Nathalie Pochet and Kota, \{Savithri Balasubramanian\} and Dan Hu and Asaf Madi and Jessica Kilpatrick and Jingwen Shi and Allen Ho and Huiyuan Zhang and Raymond Sobel and Weiner, \{Howard L.\} and Strom, \{Terry B.\} and Quintana, \{Francisco J.\} and Nicole Joller and Kuchroo, \{Vijay K.\}",
note = "Publisher Copyright: {\textcopyright} 2020 The Authors",
year = "2020",
month = jul,
day = "14",
doi = "10.1016/j.celrep.2020.107892",
language = "אנגלית",
volume = "32",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Elsevier BV",
number = "2",
}