Checkpoint Receptor TIGIT Expressed on Tim-1+ B Cells Regulates Tissue Inflammation.
Cell Rep
; 32(2): 107892, 2020 07 14.
Article
em En
| MEDLINE
| ID: mdl-32668241
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.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Especificidade de Órgãos
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Linfócitos B
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Receptores Imunológicos
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Receptor Celular 1 do Vírus da Hepatite A
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Inflamação
Limite:
Animals
Idioma:
En
Revista:
Cell Rep
Ano de publicação:
2020
Tipo de documento:
Article