Talk:Regulatory T cell
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I think that the definitions (their basic origins and proposed roles, not their molecular biology, that can be left for other sections) between TH3 (and other subsets) and Treg suppressor T cells must be clearly explained, as the former subsets are hardly or not mentioned at all. It should also be pointed out that the term "regulatory" is applied to suppressor T cells, but in reality effector T cells also regulate helper T cell responses. The terms are particularly confusing considering the TH1/TH2 model. Volantares 09:34, 19 November 2005 (UTC)
Th3 and Tr1 are just names for cell subsets that people generate in vitro. It's just a name. They may, or may not, have any relevance in vivo. I think the evidence from the IBD models is that IL-10, TGF-beta and CTLA-4 are all required for full Treg function, to greater or lesser extent. Treg are a heterogenous population which can, under different conditions, produce a wide range of cytokines. The Th1/Th2/Th17/Treg paradigm is fairly sound - each with their own transcription factor, method of differentation and key cytokines - but the Tr1 and Th3 subtypes are a little shakier. Kantokano 18:21, 15 December 2006 (UTC)
While your point about in vivo relevance is not unimportant, the current literature simply isn't capable of synthesizing those in vitro models of alternative "suppressor" populations -- thus far, the population that has the most evidence for in vivo, physiologic, and clinical application is the FoxP3+ Treg. This does not necessarily discount, or exclude the existence of Th3 or Tr1 cells, but those models simply aren't supported as well by in vivo work. I might also remind of the transwell experiments from the Shevach lab, which still support cell-contact as a necessary mechanism for classically defined Treg suppression in vitro. Jbarin 04:37, 14 January 2007 (UTC)
Perhaps it would be better for the flow of the article for it to start on with a "these are the subsets identified" section, and then continue on to the CD4+Foxp3+ Treg, which are by far the best-characterised and make up the majority of the article anyway. I'd also like to say in terms of nomenclature, "regulatory" takes preference over "supressor", so it might be better to stick to regulatory throughout. Although I'm willing to have someone argue, I haven't come across many papers or conferences with "T supressor" in the title. Kantokano 15:53, 26 September 2007 (UTC)
(reply to message above by 207.6.160.178):
RESPONSE MOVED TO IP'S TALK PAGE: User_talk:207.6.160.178
Chrisch 06:28, 11 December 2006 (UTC)
[edit] "The critical role regulatory T cells play within the immune system is evidenced by the severe autoimmune syndrome that results from a genetic deficiency in regulatory T cells."
There are environmental factors involved here too. See Hygiene Hypothesis.
- While Hygiene (capital H) continues to be a favored explanation of the contribution of environment to autoimmunity, this falls outside the scope of this article. The contribution of Tregs to control of autoimmunity need not be in any way exclusive with that of environment factors. Try appending it to Autoimmunity, in the way Allergy invokes it. Jbarin 09:44, 30 April 2007 (UTC)
I think the definitive experiment is with Scurfy or Foxp3-knockout mice - those mice develop fatal autoimmunity within a matter of weeks, where littermates or cagemates don't. Same goes for IPEX individuals. Kantokano 15:53, 26 September 2007 (UTC)
