Contribution of APCs to mucosal-associated invariant T cell activation in infectious disease and cancer

Innate Immun. 2018 May;24(4):192-202. doi: 10.1177/1753425918768695. Epub 2018 Apr 9.

Abstract

APCs such as monocytes and dendritic cells are among the first cells to recognize invading pathogens and initiate an immune response. The innate response can either eliminate the pathogen directly, or through presentation of Ags to T cells, which can help to clear the infection. Mucosal-associated invariant T (MAIT) cells are among the unconventional T cells whose activation does not involve the classical co-stimulation during Ag presentation. MAIT cells can be activated either via presentation of unconventional Ags (such as riboflavin metabolites) through the evolutionarily conserved major histocompatibility class I-like molecule, MR1, or directly by cytokines such as IL-12 and IL-18. Given that APCs produce cytokines and can express MR1, these cells can play an important role in both pathways of MAIT cell activation. In this review, we summarize evidence on the role of APCs in MAIT cell activation in infectious disease and cancer. A better understanding of the interactions between APCs and MAIT cells is important in further elucidating the role of MAIT cells in infectious diseases, which may facilitate the design of novel interventions such as vaccines.

Keywords: Antigen presenting cells; IL-12; IL-18; MAIT cell activation; MR1; cancer; infectious disease.

Publication types

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

MeSH terms

  • Antigen Presentation
  • Antigen-Presenting Cells / immunology*
  • Antigen-Presenting Cells / metabolism
  • Communicable Diseases / immunology*
  • Histocompatibility Antigens Class I / metabolism
  • Humans
  • Interleukin-12 / metabolism
  • Interleukin-18 / metabolism
  • Lymphocyte Activation*
  • Mucosal-Associated Invariant T Cells / immunology*
  • Mucosal-Associated Invariant T Cells / metabolism
  • Neoplasms / immunology*
  • Receptors, Antigen, T-Cell, alpha-beta / metabolism

Substances

  • Histocompatibility Antigens Class I
  • Interleukin-18
  • Receptors, Antigen, T-Cell, alpha-beta
  • Interleukin-12