Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer

Microbiol Mol Biol Rev. 2020 Mar 4;84(2):e00064-19. doi: 10.1128/MMBR.00064-19. Print 2020 May 20.

Abstract

Technologies allowing genetic sequencing of the human microbiome are opening new realms to discovery. The host microbiota substantially impacts immune responses both in immune-mediated inflammatory diseases (IMIDs) and in tumors affecting tissues beyond skin and mucosae. However, a mechanistic link between host microbiota and cancer or IMIDs has not been well established. Here, we propose T helper 17 (TH17) lymphocytes as the connecting factor between host microbiota and rheumatoid or psoriatic arthritides, multiple sclerosis, breast or ovarian cancer, and multiple myeloma. We theorize that similar mechanisms favor the expansion of gut-borne TH17 cells and their deployment at the site of inflammation in extraborder IMIDs and tumors, where TH17 cells are driving forces. Thus, from a pathogenic standpoint, tumors may share mechanistic routes with IMIDs. A review of similarities and divergences in microbiota-TH17 cell interactions in IMIDs and cancer sheds light on previously ignored pathways in either one of the two groups of pathologies and identifies novel therapeutic avenues.

Keywords: IL-17; IL-22; Prevotella; T helper; T helper 17; T helper cells; TH17; autoimmunity; breast cancer; cancer; cancer immunology; cancer immunotherapy; immune checkpoint; immune-mediated inflammatory disease; microbiome; microbiota; multiple myeloma; multiple sclerosis; ovarian cancer; psoriasis; regulatory T cells; rheumatoid arthritis; tumor immunology.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Immunity
  • Inflammation / complications
  • Inflammation / microbiology*
  • Mice
  • Microbiota / immunology*
  • Neoplasms / immunology
  • Neoplasms / microbiology*
  • Th17 Cells / immunology*