Aged regulatory T cells protect from autoimmune inflammation despite reduced STAT3 activation and decreased constraint of IL-17 producing T cells

Aging Cell. 2012 Jun;11(3):509-19. doi: 10.1111/j.1474-9726.2012.00812.x. Epub 2012 Mar 22.

Abstract

Regulatory T cells (Tregs) are specialized CD4(+) T lymphocytes helping defend against autoimmunity and inflammation. Although age is associated with increased inflammation and autoimmunity, few reports address age effects of immune regulation or auto-aggressive T cells. We show here that young and aged naïve CD4(+) T cells are equivalently auto-aggressive in vivo in T cell-driven autoimmune colitis. Young and aged CD4(+) Tregs equally suppressed age-matched T cell proliferation in vitro and controlled clinical and pathologic T cell-driven autoimmune colitis, suggesting equivalent regulatory function. However, whereas young and aged CD4(+) Tregs suppressed interferon (IFN)-γ(+) T cells equivalently in this model, aged CD4(+) Tregs unexpectedly failed to restrain interleukin (IL)-17(+) T cells. Nonetheless, young and aged CD4(+) Tregs equally restrained IL-17(+) T cells in vivo during acute inflammation, suggesting a chronic inflammation-related defect in aged CD4(+) Tregs. In support, aged Tregs expressed reduced STAT3 activation, a defect associated with poor IL-17-producing T cell restraint. Aged naïve mice had markedly increased programmed death (PD)-1(+) T cells, but these exhibited no significant auto-aggressive or regulatory functions in T cell-driven colitis. Young CD8(+) CD122(-) T cells induce autoimmune bone marrow failure, but we show that aged CD8(+) CD122(-) T cells do not. These data demonstrate no apparent age-related increase in auto-aggressive T cell behavior, but disclose previously unrecognized functional defects in aged CD4(+) Tregs during chronic inflammation. IL-17 can be inflammatory and contributes to certain autoimmune disorders. Reduced aged Treg function during chronic inflammation and reduced IL-17 restraint could contribute to age-related inflammation or autoimmunity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Animals
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / pathology
  • Cell Growth Processes / physiology
  • Cellular Senescence / physiology
  • Disease Models, Animal
  • Inflammation / immunology*
  • Inflammation / pathology
  • Interleukin-17 / biosynthesis*
  • Interleukin-17 / immunology
  • Mice
  • Mice, Inbred C57BL
  • STAT3 Transcription Factor / immunology*
  • STAT3 Transcription Factor / metabolism
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocytes, Regulatory / cytology
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism

Substances

  • Interleukin-17
  • STAT3 Transcription Factor
  • Stat3 protein, rat