CD4+CD25+ Regulatory T Cells Selectively Diminish Systemic Autoreactivity in Arthritic K/BxN Mice

  • Kang, Sang Mee (Department of Anatomy and Cell Biology, College of Medicine, Hanyang University) ;
  • Jang, Eunkyeong (Department of Anatomy and Cell Biology, College of Medicine, Hanyang University) ;
  • Paik, Doo-Jin (Department of Anatomy and Cell Biology, College of Medicine, Hanyang University) ;
  • Jang, Young-Ju (Laboratory of Immunology, Institute for Medical Science, Ajou University) ;
  • Youn, Jeehee (Department of Anatomy and Cell Biology, College of Medicine, Hanyang University)
  • Received : 2007.06.07
  • Accepted : 2007.09.04
  • Published : 2008.02.29

Abstract

Although the arthritis symptoms observed in the K/BxN model have been shown to be dependent on the functions of T and B cells specific to the self antigen glucose-6-phosphate isomerase, less is known about the in vivo roles of $CD4^{+}CD25^{+}$ regulatory T($T_{reg}$) cells in the pathology of K/BxN mice. We determined the quantitative and functional characteristics of the $T_{reg}$ cells in K/BxN mice. These mice contained a higher percentage of $Foxp3^+\;T_{reg}$ cells among the $CD4^+$ T cells than their BxN littermates. These $T_{reg}$ cells were anergic and efficiently suppressed the proliferation of $na\ddot{i}ve$ $CD4^+$ T cells and cytokine production by effector $CD4^+$ T cells in vitro. Antibody-mediated depletion of $CD25^+$ cells caused K/BxN mice to develop multi-organ inflammation and autoantibody production, while the symptoms of arthritis were not affected. These results demonstrate that despite the inability of the $T_{reg}$ cells to suppress arthritis development, they play a critical role protecting the arthritic mice from systemic expansion of autoimmunity.

Keywords

Acknowledgement

Supported by : MOST/KOSEF, Ministry of Health & Welfare

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