title: Interplay between effector Th17 and regulatory T cells.
abstract: BACKGROUND
  Over two decades ago, T helper cells were classified into its functional subsets. Soon after the classical observation of Mosmann et al., immunologists agreed to accept the Th1/Th2 paradigm of the T helper subsets. Each subset is not only characterized by its specific cytokines pattern and effector functions but also by their properties to counter regulate each other's functions. This classification helped to understand the complex principles of T helper cell biology and allowed us to comprehend different immune reactions in context of Th1 and Th2 subsets.
  
  
  CONCLUSIONS
  Although Th1 subsets thought to be the crucial player for most of the organ-specific autoimmune diseases like multiple sclerosis and type-1 diabetes but the loss of Th1 dominant cytokine, IFN-gamma did not prevent the development of autoimmunity which raised the possibility of involvement of other Th subsets, different from Th1 cells in the induction of autoimmunity.
  
  
  CONCLUSIONS
  Recently, a new subset of Th cells that predominantly produce IL-17 and induce autoimmunity has been discovered, and it is believed that this subset may be the major cell type involved in orchestrating tissue inflammation and autoimmunity. Recent data propose that the differentiation factors of Th17 cells reveal a link with induction of Foxp3(+) regulatory T cells. Here, we review the interplay between Th17 and Foxp3(+) T-reg cells and Tr1 cells during autoimmune inflammatory reaction.
authors.affiliation: Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, HIM 780, Boston, MA 02115, USA.
authors.forename: Amit
authors.initials: A
authors.lastname: Awasthi
authors.forename: Gopal
authors.initials: G
authors.lastname: Murugaiyan
authors.forename: Vijay K
authors.initials: VK
authors.lastname: Kuchroo
mesh_terms: D000818:Animals; D015551:Autoimmunity; D002454:Cell Differentiation / Q000276:immunology; D016207:Cytokines / Q000276:immunology*; D051858:Forkhead Transcription Factors / Q000276:immunology*; D006706:Homeostasis / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology; D020381:Interleukin-17 / Q000276:immunology*; D051379:Mice; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D016207:Cytokines; D051858:Forkhead Transcription Factors; D020381:Interleukin-17; D014157:Transcription Factors