Foxp3+ Regulatory T Cells: a Protagonist in the Ã¢ÂÂMovieÃ¢ÂÂÃ¢ÂÂ of Autoimmune Diseases?Anping Xu1, Ya Liu1,2, Bernhard Ryffel3 and Song Guo Zheng2,3*
- *Corresponding Author:
- Dr. Song Guo Zheng
2011 Zonal Ave. HMR 711, Los Angeles, CA 90033
Tel: 323 442 2128
Fax: 323 442 2874
E-mail: [email protected]
Received date: June 09, 2011; Accepted date: November 15, 2011; Published date: November 18, 2011
Citation: Xu A, Liu Y, Ryffel B, Zheng SG (2011) Foxp3+ Regulatory T Cells: a Protagonist in the "Movie'' of Autoimmune Diseases? Rheumatology 1:e102. doi: 10.4172/2161-1149.1000e102
Copyright: © 2011 Xu A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Although CD4+CD25+Foxp3+ regulatory or suppressor T cells (Tregs) play a crucial role in the maintenance of self-tolerance and immune homeostasis against self-antigen, the true role they play in autoimmune diseases is still less defined. The prospect for therapeutic roles of these cells in autoimmune diseases is somehow fuzzy. This editorial will discuss and update these issues and proposes several new directions to address the relative concerns. Thymus-derived, naturally-occurring CD4+CD25+ suppressor cells (nTregs) were originally described by Sakaguchi and his colleagues where they identified that CD4+CD25+ cells in the thymus are crucial for the control of autoimmunity . As CD25 is also activation marker for lymphocytes and therefore its expression is unable to exclude other T effector (Teff) cell population that may contaminate Tregs. Subsequent studies have demonstrated that Foxp3, a member of the forkhead/ winged-helix family of transcription factors, is essentially important for the differentiation and function of Tregs, and is considered as the best marker for their phenotypic identification so far [2-4]. Mutation or disruption of the Foxp3 (in mouse) or FOXP3 (in human, an analogue of Foxp3 in mouse) gene resulted in fatal lymphoproliferative disorder in mice, and a severe multiple autoimmune disease called immune dysregulation, polyendocrinopathy, enteropathy X-linked syndrome (IPEX) in humans [5-7]. The abnormality in the numbers and function of Tregs in the periphery has been widely associated with the development and progression of many autoimmune diseases.