T-cell selection and intestinal homeostasis

Immunol Rev. 2014 May;259(1):60-74. doi: 10.1111/imr.12171.


Although intestinal bacteria live deep within the body, they are topographically on the exterior surface and thus outside the host. According to the classic notion that the immune system targets non-self rather than self, these intestinal bacteria should be considered foreign and therefore attacked and eliminated. While this appears to be true for some commensal bacterial species, recent data suggest that the immune system actively becomes tolerant to many bacterial organisms. The induction or activation of regulatory T (Treg) cells that inhibit, rather than promote, inflammatory responses to commensal bacteria appears to be a central component of mucosal tolerance. Loss of this mechanism can lead to inappropriate immune reactivity toward commensal organisms, perhaps contributing to mucosal inflammation characteristic of disorders such as inflammatory bowel disease.

Keywords: T cell; T-cell receptors; inflammatory bowel disease; mucosa.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bacteria / immunology
  • Cell Differentiation / immunology
  • Cellular Microenvironment / immunology
  • Clonal Selection, Antigen-Mediated / immunology*
  • Dendritic Cells / immunology
  • Epitopes, T-Lymphocyte / immunology
  • Homeostasis / immunology*
  • Host-Pathogen Interactions / immunology
  • Humans
  • Immune System / immunology
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / metabolism
  • Inflammatory Bowel Diseases / microbiology
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / microbiology
  • Intestines / immunology*
  • Intestines / microbiology
  • T-Lymphocytes, Regulatory / cytology
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism
  • T-Lymphocytes, Regulatory / microbiology
  • Transcription Factors / metabolism


  • Epitopes, T-Lymphocyte
  • Transcription Factors