Regulatory T cell activation, proliferation, and reprogramming induced by extracellular vesicles

J Heart Lung Transplant. 2021 Nov;40(11):1387-1395. doi: 10.1016/j.healun.2021.06.005. Epub 2021 Jun 24.

Abstract

Background: Extracellular vesicles (EVs) from heart stromal/progenitor cells modulate innate immunity, with salutary effects in a variety of cardiac disease models. Little is known, however, about the effects of these EVs on adaptive immunity.

Methods: Ex vivo differentiation of naïve CD4+ T cells was conducted to assess the effect of EVs on cytokine production and proliferation of Th1, Th2, Th17, and regulatory T (Treg) cells. These effects were further tested in vivo using the experimental autoimmune myocarditis (EAM) model.

Results: Using differentiated CD4+ T cells, we show that EVs secreted by human-derived heart stromal/progenitor cells selectively influence the phenotype, activity, and proliferation of regulatory T (Treg) cells. Exposure of Treg cells to EVs results in faster proliferation, augmented production of IL-10, and polarization toward an intermediate FOXP3+RORγt+ phenotype. In experimental autoimmune myocarditis, EVs attenuate cardiac inflammation and functional decline, in association with increased numbers of splenic IL10+-Treg cells.

Conclusions: T cell modulation by EVs represents a novel therapeutic approach to inflammation, harnessing endogenous immunosuppressive mechanisms that may be applied in solid organ transplantation, graft-versus-host disease, and autoimmune disorders.

Keywords: CD4(+) T cells; extracellular vesicles; inflammation, regulatory T cells.

Publication types

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

MeSH terms

  • Adaptive Immunity / immunology*
  • Animals
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / pathology
  • Cell Differentiation
  • Cell Proliferation
  • Cells, Cultured
  • Cytokines / metabolism
  • Disease Models, Animal
  • Extracellular Vesicles / metabolism*
  • Female
  • Immunity, Innate*
  • Lymphocyte Activation / immunology*
  • Mice
  • Myocarditis / immunology*
  • Myocarditis / pathology
  • Rats
  • Rats, Inbred Lew
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / pathology

Substances

  • Cytokines