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Tregs may also be low in subsets

nandixon

Senior Member
Messages
1,092
I was trying to find this test at Labcorp...is it just CD3+CD25? The only panel I can find is called a Tcell activation panel but not sure that is the same thing he referenced on selfhacked?
Selfhacked doesn't provide the actual test needed, and the T-Cell Activation Profile that LabCorp offers doesn't include the necessary test.

To help determine your Treg status, I think you'd probably want to at least test for the commonest version of Tregs (as it's currently understood), i.e., the CD4+CD25+FoxP3+ subset of T cells.

Mayo offers a test for this, although they seem to sort of cheat and measure CD127 as a proxy for FoxP3:
http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/89318

I'd be curious if this specific testing for Tregs is in fact also available through LabCorp or Quest Diagnostics. And if not, why not. (It may be a demand issue, or a difficulty issue.)

Testing that does not include the FoxP3 marker (or a proxy) will not be sufficient, I don't think, to let a person know what might be going on with their Tregs (and even then this doesn't take into account differences that might exist in Treg populations in the peripheral blood versus specific tissues, e.g., the spleen).
 

Ema

Senior Member
Messages
4,729
Location
Midwest USA
Selfhacked doesn't provide the actual test needed, and the T-Cell Activation Profile that LabCorp offers doesn't include the necessary test.

To help determine your Treg status, I think you'd probably want to at least test for the commonest version of Tregs (as it's currently understood), i.e., the CD4+CD25+FoxP3+ subset of T cells.

Mayo offers a test for this, although they seem to sort of cheat and measure CD127 as a proxy for FoxP3:
http://www.mayomedicallaboratories.com/test-catalog/Clinical and Interpretive/89318

I'd be curious if this specific testing for Tregs is in fact also available through LabCorp or Quest Diagnostics. And if not, why not. (It may be a demand issue, or a difficulty issue.)

Testing that does not include the FoxP3 marker (or a proxy) will not be sufficient, I don't think, to let a person know what might be going on with their Tregs (and even then this doesn't take into account differences that might exist in Treg populations in the peripheral blood versus specific tissues, e.g., the spleen).
Selfhacked recommends this test panel:

http://www.truehealthlabs.com/Natural-Killer-Cell-and-Activated-T-Cell-Profile-p/lc_502500.htm
 

Ema

Senior Member
Messages
4,729
Location
Midwest USA
@Ema, that test panel doesn't specifically test for the FoxP3+ Tregs in question.
I know but that was why I selected the panel I did from Labcorp.

I admit I don't know enough about this to understand why the FoxP3+ marker is critical over just measuring the tregs as a whole.
 

nandixon

Senior Member
Messages
1,092
@Ema, the FoxP3 marker is what actually defines a Treg, or at least the most common variety (as it's currently understood). Testing for anything else means a person is trying to infer what their Treg status is, and that inference could be wrong.
 

Ema

Senior Member
Messages
4,729
Location
Midwest USA
This helps some (but not all!).

Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease.
Review article
Sakaguchi S, et al. Immunol Rev. 2006.
Show full citation
Abstract
Naturally arising CD25+ CD4+ regulatory T (Treg) cells, most of which are produced by the normal thymus as a functionally mature T-cell subpopulation, play key roles in the maintenance of immunologic self-tolerance and negative control of a variety of physiological and pathological immune responses. Natural Tregs specifically express Foxp3, a transcription factor that plays a critical role in their development and function. Complete depletion of Foxp3-expressing natural Tregs, whether they are CD25+ or CD25-, activates even weak or rare self-reactive T-cell clones, inducing severe and widespread autoimmune/inflammatory diseases. Natural Tregs are highly dependent on exogenously provided interleukin (IL)-2 for their survival in the periphery. In addition to Foxp3 and IL-2/IL-2 receptor, deficiency or functional alteration of other molecules, expressed by T cells or non-T cells, may affect the development/function of Tregs or self-reactive T cells, or both, and consequently tip the peripheral balance between the two populations toward autoimmunity. Elucidation of the molecular and cellular basis of this Treg-mediated active maintenance of self-tolerance will facilitate both our understanding of the pathogenetic mechanism of autoimmune disease and the development of novel methods of autoimmune disease prevention and treatment via enhancing and re-establishing Treg-mediated dominant control over self-reactive T cells.