Inflammatory effects of ex vivo human Th17 cells are suppressed by regulatory T cells

J Immunol. 2010 Sep 15;185(6):3199-208. doi: 10.4049/jimmunol.1000557. Epub 2010 Aug 18.

Abstract

Th17 cells are proinflammatory cells associated with many immune-mediated diseases. Major factors limiting the study of human Th17 cells are the lack of an accepted method for their in vitro differentiation or for isolation of a homogenous population of Th17 cells that do not cosecrete IFN-gamma. To overcome these hurdles, we established a novel method to isolate in vivo differentiated Th17 cells from peripheral blood by sorting CD161(+)CCR4(+)CCR6(+)CXCR3(-)CD4(+) T cells. The resulting cells produce high levels of IL-17 but not IFN-gamma, express high levels of retinoic acid-related orphan receptor variant 2, and maintain this phenotype upon expansion. Ex vivo Th17 cells exhibit a low cytotoxic potential and are hyporesponsive to polyclonal anti-CD3/anti-CD28 stimulation. Importantly, ex vivo Th17 cells were susceptible to suppression by both naive and memory regulatory T cells (Tregs), which inhibited production of IL-17, IL-22, and CXCL8. Moreover, Tregs suppressed the antifibrotic effects of Th17 cells in a wound-healing model. These findings provide new tools for the study of normal and pathological functions of bona fide Th17 cells in humans. They also provide new insight into the cross-talk between Th17 cells and immune and nonimmune cells, and they establish the paradigm that adoptive Treg-based therapies may effectively limit Th17-mediated inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation / immunology
  • Cell Proliferation
  • Cell Separation / methods
  • Cells, Cultured
  • Coculture Techniques
  • Down-Regulation / immunology*
  • Flow Cytometry / methods
  • Humans
  • Immunophenotyping
  • Inflammation / immunology
  • Inflammation / pathology
  • Inflammation / prevention & control
  • Inflammation Mediators / physiology*
  • Interleukin-17 / antagonists & inhibitors
  • Interleukin-17 / metabolism
  • Interleukin-17 / physiology*
  • Interleukin-22
  • Interleukin-8 / antagonists & inhibitors
  • Interleukin-8 / biosynthesis
  • Interleukins / antagonists & inhibitors
  • Interleukins / biosynthesis
  • T-Lymphocytes, Helper-Inducer / immunology*
  • T-Lymphocytes, Helper-Inducer / metabolism
  • T-Lymphocytes, Helper-Inducer / pathology
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism
  • T-Lymphocytes, Regulatory / pathology
  • Wound Healing / immunology

Substances

  • CXCL8 protein, human
  • Inflammation Mediators
  • Interleukin-17
  • Interleukin-8
  • Interleukins