Inflammation-associated genes: risks and benefits to Foxp3+ regulatory T-cell function

Immunology. 2015 Oct;146(2):194-205. doi: 10.1111/imm.12507. Epub 2015 Sep 9.

Abstract

Foxp3(+) regulatory T (Treg) cells prevent the development of autoimmunity and immunopathology, as well as maintaining homeostasis and tolerance to commensal microorganisms. The suppressive activity of Treg cells is their defining characteristic, generating great interest in their therapeutic potential. However, suppressive and effector functions are not entirely exclusive. Considerable evidence points to the ability of supposedly anti-inflammatory Foxp3-expressing Treg cells to also express transcription factors that have been characterized as cardinal drivers of T effector cell function. We will consider the mounting evidence that Treg cells can function in non-suppressive capacities and review the impetus for this functional change, its relevance to developing immune and autoimmune responses and its significance to the development of Treg-based therapies.

Keywords: Foxp3; autoimmunity; cytokine receptors; cytokines; regulatory T cells; transcription factors.

Publication types

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

MeSH terms

  • Animals
  • Cytokines / genetics
  • Cytokines / immunology*
  • Cytokines / metabolism
  • Forkhead Transcription Factors / immunology*
  • Forkhead Transcription Factors / metabolism
  • Genetic Markers
  • Genetic Predisposition to Disease
  • Humans
  • Immunophenotyping
  • Inflammation / genetics
  • Inflammation / immunology*
  • Inflammation / metabolism
  • Inflammation / therapy
  • Inflammation Mediators / immunology*
  • Inflammation Mediators / metabolism
  • Phenotype
  • Receptors, Cytokine / genetics
  • Receptors, Cytokine / immunology*
  • Receptors, Cytokine / metabolism
  • T-Lymphocytes, Helper-Inducer / immunology
  • T-Lymphocytes, Helper-Inducer / metabolism
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / immunology*
  • Transcription Factors / metabolism

Substances

  • Cytokines
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Genetic Markers
  • Inflammation Mediators
  • Receptors, Cytokine
  • Transcription Factors