IL-37 Represses the Autoimmunity in Myasthenia Gravis via Directly Targeting Follicular Th and B Cells

J Immunol. 2020 Apr 1;204(7):1736-1745. doi: 10.4049/jimmunol.1901176. Epub 2020 Feb 28.

Abstract

IL-37 is a newly identified immune-suppressive factor; however, the function, cellular sources, and mechanism of IL-37 in humoral immunity and Myasthenia gravis (MG) are still unclear. In this study, we found IL-37 were substantially downregulated in the serum and PBMCs of MG patients compared with healthy controls. The lower IL-37 was associated with severer disease (quantitative MG score) and higher follicular Th (Tfh)/Tfh17 and B cell numbers. Flow cytometry analysis revealed that IL-37 was mainly produced by CD4+ T cells without overlapping with Th1, Th17, and Tfh subsets in MG patients. Regulatory IL-37+ T cell rarely expressed Foxp3 and CD25 but produced numerous IL-4. Tfh and B cell expressed high levels of SIGIRR, the receptor of IL-37, in MG patients. Mechanically, IL-37 directly bond to SIGIRR, repressed the proliferation, cytokine production of Tfh and B cells, and the secretion of autoantibody via inhibition of STAT3 signaling in Tfh and B cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Autoantibodies / immunology
  • Autoimmunity / immunology*
  • B-Lymphocytes / immunology*
  • Cells, Cultured
  • Female
  • Humans
  • Immunity, Humoral / immunology
  • Interleukin-1 / immunology*
  • Male
  • Middle Aged
  • Myasthenia Gravis / immunology*
  • T-Lymphocytes, Helper-Inducer / immunology*
  • Th17 Cells / immunology*

Substances

  • Autoantibodies
  • IL37 protein, human
  • Interleukin-1