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- 1 subsets
- 2 T cell maturation
- 3 Maturation paradox
- 4 Th40 cells
- 5 Tregs
- 6 Cytotoxic T Cells
- 7 γδ T cells
- 8 Hyphen or not?
- 9 Differential signaling
- 10 T cell Differentiation
- 11 T Cells, vitamin D3 (cholecalciferol), calcidiol, and calcitriol
- 12 Positive selection
- 13 Activation
- 14 Should mention MAIT cells
- 15 Consistent capitalization
Could we clarify if the listed subsets are distinct or overlapping. If overlapping then we could add CD4+ T cells and CD8+ T cells as they often refered to. It's not clear if there are 2 or 4 subtypes of memory T cells. Rod57 (talk) 13:14, 23 January 2008 (UTC)
T cell maturation
- Yes, I agree...someone should do this...It basically says the same thing at parts...Dan (talk) 23:16, 1 April 2008 (UTC)
This chapter makes no sense. First of all, during the first positive selections only T cell capable of binbding to MHC are selcted. During second negative selction all auto-reactive T cells are killed, meaning: T cell that are activated by self-antigens in MHC are killed (self-antigens are presented in the thymus for this reason). Therfore, there is no paradox. All other T cells survive. The real paradox is, how T cell mediated autoimmunity arises despite these selction methods (e.g. multiple sclerosis). At this point the authors "differential avidity hypothesis" could probably fit (autoreactive T cells survive because of weak / too strong binding). However, even this is still a hypothesis and discussed in the specialists literature. Furthermore, the author asks: "How do we have immunity at all?" Of course, there is not only T cell mediated immunity! Also, not a signle citation is given. The two other wiki pages that are linked in this chapter are rudimentary stubs, also without any citations. I don't belive it and suggest to delete it.
I've never heard of this nomenclature, and I can't find anything on Pubmed or google for "Th40" cells. It seems that the process described does occur, but I don't know of its relevance and it seems to be more of a mechanism of tolerance rather than an individual T cell subset. If someone can come up with some decent papers to show the opposite, I'm willing to be persuaded, otherwise it'll have to be deleted. Kantokano (talk) 14:54, 22 November 2007 (UTC)
Does anyone know for sure if regulatory T cell is just a newer name for suppressor T cell, or if there is still some distinction between them? I would like to combine them under one article for regulatory t cell and relink it to this page. What do you think? Wiccan Quagga 16:40, 6 Feb 2005 (UTC)
Well according to my 3rd year Immunology lecturer T_regs are definitely not the same as T_suppresors. If anything you might consider suppressor T cells a subset of regulatory T cells T_suppressors were the subject of much research in the 1980's but fell into some trouble and a coherent model was not established. A paper by Sakaguchi in 1995 revived interest in the idea when CD25+ CD4+ T cells were demonstrated to show suppressor function. These could be thought of as 'natural' suppressor cells since other T cells also display suppressor funtion, namely CD4+ CD25- Tr1 cells and Th3 cells. --schroding79 04:00, 22 September 2006 (UTC)
A slightly different historicism: To hear Ethan Shevach talk about the canonical CD4+CD25+FoxP3+ Treg, it's pretty much synonymous. To my understanding, the original "suppressor T" from the 70s literature simply didn't withstand the scrutiny of molecular characterization. When the Mosmann & Coffman Th1/Th2 model broke in the mid-80s, the "suppressor" model was thought to simply reflect the counterregulation of those populations. Jbarin 11:34, 21 November 2006 (UTC)
Cytotoxic T Cells
someone might want to mention a few things about cytotoxic T cells. I think that most people tend to think of these cells when thinking of T cells. wikipedia already has an article for them. http://en.wikipedia.org/wiki/Cytotoxic_t_cell
- The cytotoxic T cell section used to be there, but got hit by a vandal and went unnoticed...thanks for drawing this to our attention!! I put it back. Ciar 05:30, 22 May 2007 (UTC)
"Through SLOB[clarification needed] interaction with T regulatory CD4+CD25+FoxP3+ cells, these cells can be inactivated to a anergic state, which prevent autoimmune diseases such as experimental autoimmune encephalomyelitis."
- At least in mice (the most common model) activley induced EAE is almost completly CD4-mediated. Inactivating CD8 cells would lead to nothing. ghm... citation: type "EAE mice" in pubmed. Almost every introduction contains this. —Preceding unsigned comment added by 126.96.36.199 (talk) 14:47, 18 June 2009 (UTC)
γδ T cells
The name looks weird but a quick Google seems to confirm it. Any info on γδ T cells would be great. Kevs 02:19, 29 August 2006 (UTC)
Updated on main page --schroding79 04:00, 22 September 2006 (UTC) Classical suppressor cells expressed the CD8 marker (same one as expressed by cytotoxic T lymphocytes). Richard Gershon (Yale University) was a pioneer researcher in this area. The field of suppressor (and "contrasuppressor") T cells became controversial and discredited when the restriction (MHC) elements and mechanism (suppressor factors) could not be elucidated.
Hyphen or not?
Throughout the article the term is spelled without a hyphen (T cell), except in the accompanying image for T cell activation, where it's inconsistently spelled "T-cell" and "T cell" - Can someone clarify the usage here? Is with or without hyphen preferred? Should there be a difference for hyphenated adejctives, as in "T-cell activation"?
Thanks, 188.8.131.52 14:30, 10 September 2007 (UTC)
It's not really a set phrase, so rules are as for normal hyphen usage. I'd just go with whatever makes sense at the time. Unless it's unclear that the "cell" refers to the "T", I'd stick with "T cell". But in some cases, as with "T-cell activation", where, to the non-specialist, there is the potential for confusion as to what is happening, I'd use a hyphen. Consult a copy of Fowler's! Kantokano 15:15, 10 September 2007 (UTC)
- Thanks for clarifying! 184.108.40.206 16:17, 21 September 2007 (UTC)
- Sorry Dan, but I just thought it best to remove the link altogether since it (and the "poor" stub link above it) were not completely relevant to T cell anyway! ~ Ciar ~ (Talk to me!) 00:15, 28 March 2008 (UTC)
T cell Differentiation
- The page is pretty much still in its infancy, it seems, and needs a lot of TLC to add in a wealth of missing info. It could do with a regular editor to adopt it and build it up into a good article. If you up to the challenge, why not take it on Dan! :o) ~ Ciar ~ (Talk to me!) 01:14, 2 April 2008 (UTC)
T Cells, vitamin D3 (cholecalciferol), calcidiol, and calcitriol
I want to add the latest research findings on the relationship between vitamin D and T-cells, though my edits are being deleted by the community; perhaps because I need some help from the community to understand the best way to include this new information. Below are my findings.
The main things that this article should reflect, but currently doesn't:
1. The T-cell is one of many activation centers for calcidiol, meaning that the T-cell expresses the CYP27B1 gene, and turns the pre-hormone calcidiol into the seco-steroid hormone calcitriol. 
2. T-cells themselves are actually activated by calcitriol; there's a very "symbiotic" relationship, for lack of a better word. The T-cell expresses CYP27B1, which allows for calcidiol to be activated and turned into calcitriol. Then calcitriol activates the T-cell, allowing it to do its work.
When a T cell is exposed to a foreign pathogen, it extends a VDR with which it searches for calcitriol; if an insufficient amount of calcitriol is in the area, the T-cell remains dormant.
- Sigmundsdottir H, Pan J, Debes GF, Alt C, Habtezion A, Soler D, Butcher EC (March 2007). "DCs metabolize sunlight-induced vitamin D3 to 'program' T cell attraction to the epidermal chemokine CCL27". Nat. Immunol. 8 (3): 285–93. doi:10.1038/ni1433. PMID 17259988.
- Another reason vitamin D is important: It gets T cells going
- Marina Rode von Essen, Martin Kongsbak, Peter Schjerling, Klaus Olgaard, Niels Ødum & Carsten Geisler (2010). "Vitamin D controls T cell antigen receptor signaling and activation of human T cells". Nature Immunology (11): 344–349. doi:10.1038/ni.1851.
- I do not see any problem of mentioning the role of vitamin D in T cell activation. However vitamin D should not be given undue weight. While it is true that "T-cell is one of many activation centers for calcidiol", it is equally true that "calcidiol is only one of many factors necessary for T cell activation". To imply that vitamin D is a key activator of T cells is misleading. It is more accurate to say that vitamin D is a necessary but insufficient condition for T cell activation. The key (i.e., first) step in activation is binding of TCR to an antigen. Furthermore "signalling pathways downstream from both CD28 and the T cell receptor involve many proteins" and the expression of a subset of these proteins in regulated by calcitriol activated VDR (for more detail see Naive_T_cell#Mechanism_of_activation). Hence I would not object if a short paragraph concerning the role of vitamin D in the activation T cells were added to the end of the T_cell#Activation section but the first paragraph of this section as it is currently written should be retained. Boghog (talk) 11:57, 3 January 2011 (UTC)
- I understand that T-cell activation is a complex process and there are many proteins and pathways involved, though I disagree that saying "vitamin D is a key activator" is misleading. I've got some detailed thoughts on this but need to think them through before I respond. Sorry I can't give a full response now, but school's taking up most of my time right now. Cheers, Adam C (talk) 22:03, 10 February 2011 (UTC)
- Thanks for adding the paragraph on Vitamin D. I have edited it somewhat to mention that vitamin D is part of a delayed response mechanism and added more detailed explanation of the role it plays. I have also removed the "extended antenna" VDR analogy since this implies that VDR exists in naive T cells and moved to the cell surface when the T cell is activated. What actually happens is that VDR levels are very low in naive T cells but levels of VDR increase when the T cell is activated. Furthermore, VDR resides in the nucleus regardless of whether it is bound to calitriol or not. Boghog (talk) 16:30, 12 February 2011 (UTC)
- Vitamin D is just not a major factor and doesn't deserve the kind of focus it's been given. Maybe one sentence, but not a paragraph. If you wrote a paragraph on every factor that has at some point been described to influence T cells, this article would go on for hundreds of pages. Vitamin D is not the "on switch" for T cells, TCR is. The papers you've cited are really about avidity maturation than anything about calcitriol being a fundamental on/off switch for T cells. This section (as I wrote it) is really about initial naive T cell activation than avidity maturation - maybe there should be another article on that kind of thing. — Preceding unsigned comment added by Kantokano (talk • contribs) 03:23, 19 February 2012 (UTC)
- I think that they also continue to rearrange their α chains - and so have further chances to be positively selected - this isn't compatible with the idea that they undergo apoptosis if they don't receive the survival signal straight away. Hamdev (talk) 21:04, 14 December 2011 (UTC)
The figure in the activation section is erroneous, unreferenced and very confusing. I would delete it but I stopped waiting a urgent reply by the author; today is june 26 2012. The figure must be substitued or corrected and referenced. T cells in the section text are CD4+ while in the figure they are simply labelled "T cells". MHC class of the stimulation complex is unclear and confusing. The figure shows what appears a switch cytotoxic-helper function unclear and possibly in contrast with current paradigms. — Preceding unsigned comment added by Roberto90967 (talk • contribs) 13:21, 26 July 2012 (UTC)
Should mention MAIT cells
Since 2009 there has been discussion of mucosal-associated invaraint T cells which seem to be activated by molecules presented by MR1 on antigen presenting cells. Should at least mention them here, then give them their own article. eg MR1 antigen presentation to mucosal-associated invariant T cells was highly conserved in evolution. 2009, [http://www.nature.com/icb/journal/v88/n8/full/icb2010104a.html Innate T cells detect bacteria. Bacteria, mucosal-associated invariant T cells and MR1. 2010], MR1 presents microbial vitamin B metabolites to MAIT cells. 2012 - Rod57 (talk) 03:12, 1 December 2012 (UTC)
The problem is the balance between making a truly comprehensive article and a readable one - I've been trying for a while to stop this article drifting off into the latest and strangest subset and to keep it general and not involve every paper someone has read and decided is important. It's probably worth waiting until these cells have been better outlined before adding them. --Kantokano (talk) 06:06, 3 January 2013 (UTC)
If "T-sub-H" and "T-sub-h" refer to the same object, the article should consistently use one of the two conventions. Same for "T-sub-c" and "T-sub-C". If they do not refer to the same object, the article should specify what a "T-sub-h" cell is.