Commensal regulation of T cell survival through Erdr1

Gut Microbes. 2018;9(5):458-464. doi: 10.1080/19490976.2018.1441662. Epub 2018 Apr 11.

Abstract

The commensal microbiota influences many aspects of immune system regulation, including T cells, but molecular details of how this occurs are largely unknown. Here we review our findings that the microbiota regulates Erdr1, a secreted apoptotic factor, to control T cell survival. Erdr1 is highly upregulated in CD4+ T cells from germfree mice and antibiotic treated animals, and our study shows that Erdr1 is suppressed by the microbiota via Toll-like receptor signaling and MyD88 dependent pathways. Erdr1 functions in an autocrine fashion and promotes apoptosis through the FAS/FASL pathway. Suppression of Erdr1 leads to survival of autoreactive T cells and exacerbated autoimmune disease in the EAE model, and overexpression of Erdr1 results in lessened disease. This novel T cell apoptotic factor has implications for autoimmunity, cancer biology, and invasive pathogens and thus represents a novel therapeutic target in disease.

Keywords: Erdr1; Host-pathogen interactions; T cells; TLRs; autoimmunity; microbiota.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Survival
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Encephalomyelitis, Autoimmune, Experimental / microbiology
  • Gastrointestinal Microbiome*
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / immunology*
  • Mice
  • Symbiosis
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / immunology
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / immunology*

Substances

  • Membrane Proteins
  • Tumor Suppressor Proteins
  • erythroid differentiation regulator 1, mouse