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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

Peroxisome proliferator-activated receptor gamma is required for regulatory CD4+ T cell-mediated protection against

Raquel Hontecillas1, Josep Bassaganya-Riera

  • 1Laboratory of Nutritional Immunology and Molecular Nutrition, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. magarzo@vt.edu

Journal of Immunology (Baltimore, Md. : 1950)
|February 22, 2007
PubMed

Insights

Endogenous Peroxisome proliferator-activated receptor (PPAR) gamma activation in regulatory T cells (Tregs) suppresses effector T cell function and prevents colitis. Loss of PPAR gamma in Tregs impairs their protective role, leading to enhanced inflammation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Peroxisome proliferator-activated receptor (PPAR) gamma is linked to preventing immunoinflammatory disorders.
  • The precise role of endogenous PPAR gamma in regulating CD4+ T cell functions, particularly effector and regulatory T cells (Tregs), remains incompletely understood.

Purpose of the Study:

  • To investigate the function of endogenous PPAR gamma in CD4+ T cell populations.
  • To elucidate the role of PPAR gamma in the suppressive capacity of regulatory T cells (Tregs) and the development of colitis.

Main Methods:

  • Utilized PPAR gamma-deficient CD4+ T cells from tissue-specific null mice (PPAR gamma fl/fl; MMTV-Cre+).
  • Assessed Ag-specific proliferation and IFN-gamma production in response to IL-12.
  • Evaluated disease susceptibility in vivo using trinitrobenzene sulfonic acid-induced colitis models.
  • Performed adoptive transfer studies of PPAR gamma-deficient and wild-type T cells into SCID recipients.

Main Results:

  • Loss of PPAR gamma led to increased Ag-specific T cell proliferation and IFN-gamma overproduction.
  • PPAR gamma-deficient mice showed heightened susceptibility to chemically induced colitis.
  • Transfer of PPAR gamma-null CD4+ T cells into SCID recipients induced enteric disease.
  • PPAR gamma-expressing Tregs, but not PPAR gamma-null Tregs, prevented colitis in cotransfer studies.
  • IFN-gamma production by CD4+ T cells was reduced by PPAR gamma-expressing Tregs.

Conclusions:

  • Endogenous PPAR gamma activation is an intrinsic mechanism within Tregs that down-regulates effector CD4+ T cell activity.
  • PPAR gamma expression in Tregs is crucial for preventing colitis development.
  • These findings highlight a key regulatory pathway for maintaining gut immune homeostasis.

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