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Checkpoint Receptor TIGIT Expressed on Tim-1+ B Cells Regulates Tissue Inflammation.

Sheng Xiao1, Lloyd Bod1, Nathalie Pochet1

  • 1Evergrande Center for Immunologic Diseases and Ann Romney Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.

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|July 16, 2020
PubMed
Summary
This summary is machine-generated.

Tim-1 and TIGIT on B cells prevent tissue inflammation and paralysis. Tim-1 signaling regulates TIGIT and IL-10 production, crucial for central nervous system (CNS) tolerance.

Keywords:
AutoimmunityB cellsSpontaneous inflammatory disordersTIGITTim-1Tissue tolerance

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Area of Science:

  • Immunology
  • Neuroscience

Background:

  • Tim-1 (T cell immunoglobulin and mucin-domain containing-1) is a phosphatidylserine receptor on B cells.
  • Tim-1 senses apoptotic cells, inducing interleukin-10 (IL-10) production.

Purpose of the Study:

  • To investigate the role of Tim-1 and TIGIT in B cells for maintaining self-tolerance.
  • To explore the regulatory mechanisms of B cell function, including the potential role of the aryl hydrocarbon receptor (AhR).

Main Methods:

  • B cell-specific gene deletion of Tim-1 and TIGIT in mice.
  • Transcriptomic analysis of B cells.
  • Assessment of tissue inflammation and central nervous system (CNS) pathology.

Main Results:

  • B cell-specific Tim-1 deletion led to multi-organ inflammation and CNS paralysis.
  • Tim-1+ B cells express co-inhibitory checkpoint receptors, including TIGIT.
  • B cell-specific TIGIT deletion caused CNS inflammation and paralysis, but limited peripheral inflammation.
  • Aryl hydrocarbon receptor (AhR) was preferentially expressed in Tim-1+ B cells and regulated TIGIT and IL-10 expression.

Conclusions:

  • Tim-1+ B cells are critical for maintaining self-tolerance and limiting tissue inflammation.
  • Tim-1 signaling-dependent TIGIT expression on B cells is essential for CNS-specific tolerance.
  • AhR plays a regulatory role in B cell function, influencing TIGIT and IL-10 expression.