Revisiting the old link between infection and autoimmune disease with commensals and T helper 17 cells

J. Magarian Blander, Miriam B. Torchinsky, Laura Campisi

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

Abstract

Genetic composition and major histocompatibility complex polymorphisms unequivocally predispose to autoimmune disease, but environmental factors also play a critical role in precipitating disease in susceptible individuals. Notorious among these has been microbial infection. Older studies describing associations between microbial infection and autoimmune disease are now followed by new studies demonstrating correlations between susceptibility to autoimmune disease and commensal colonization of the intestinal tract. T helper 17 (T H17) cells have gained a prominent role in autoimmune disease, and notably, their development within the intestine has been linked to colonization with specific commensal bacteria. Here, we consider current views on how microbes, TH17 cells, and autoimmunity are connected. We speculate on how the intricate relationships among commensal, pathogen, and the host might ultimately determine susceptibility to autoimmune disease.

Original languageEnglish
Pages (from-to)50-68
Number of pages19
JournalImmunologic Research
Volume54
Issue number1-3
DOIs
StatePublished - Dec 2012

Keywords

  • Antigen presentation
  • Autoimmune disease
  • Autoimmunity
  • Autoreactivity
  • B cell
  • CD4 T cell
  • Central tolerance
  • Commensal
  • Germ free
  • Host-commensal interaction
  • Host-pathogen interaction
  • Infection
  • Inflammatory bowel disease
  • Innate immunity
  • Lymphocyte
  • MHC
  • Major histocompatibility complex
  • Multiple sclerosis
  • Nod-like receptor
  • Pathogen
  • Peripheral tolerance
  • Rheumatoid arthritis
  • Specific pathogen free
  • T cell
  • T helper 17
  • Toll-like receptor
  • Type 1 diabetes mellitus

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