ME/CFS and Tregs - confused

[nandixon]

Yes, the elevation of Tregs might be adaptive.

However, rituximab seems to upregulate Tregs.

I didn't think it had any effect:

The anti-CD20 antibody rituximab reduces the Th17 cell response

From the Discussion section:

In the present study we demonstrated that rituximab inhibits the Th17 response in humans. Rituximab reduces the local Th17 response in patients with RA, and this is associated with a decrease in inflammation and better clinical outcome. Interestingly, the effect of rituximab is Th17 specific, since rituximab had no effects on Treg cell, Th1 cell, or TNF responses. Inhibition of the Th17 response by rituximab is lost in the absence of B lymphocytes. These findings provide strong evidence that B cells are able to modulate the Th17 response, and rituximab inhibits the Th17 function through B cell depletion.

(Btw, the above study cites Prof. Edwards 2004 NEJM study as reference #1. )

 

[adreno]

I didn't think it had any effect:

The anti-CD20 antibody rituximab reduces the Th17 cell response

Patients, particularly responders, showed restored numbers of Tregs as well as a restored regulatory function upon treatment with rituximab.

http://www.ncbi.nlm.nih.gov/pubmed/18375792

In addition, both groups experienced a significant up-regulation in Treg cell levels, but the up-regulation in the experimental group was maintained at an even higher level and persisted a longer time than those in the glucocorticoids group.

http://www.ncbi.nlm.nih.gov/pubmed/21188563

 

[nandixon]

@adreno, I've seen that article before and I interpreted the increase in Tregs as being due to their being abnormally low to begin with:

Pretreatment data revealed a reduced number and a defective suppressive capacity of Tregs in ITP patients compared with control individuals.

EDIT: And the same seems true for the second reference as well.

 

[anciendaze]

Based on what we know from other work there are two problems with this research: a need to distinguish stages of pathology in which regulation may be different; failure to distinguish between natural and inducible T-regs, which are important indicators of immune senescence. I can't emphasize enough that immune response is a highly dynamic process in which looking for measures which remain static while ignoring context disregards vital information.

Traditional medical research techniques have barely coped with humoral immune response. When it comes to cellular components of immune response we are still groping in the dark.

 

[Jonathan Edwards]

All fairy tales to my mind. The stuff on RA does not make any real sense to me. Abnormalities of immune response in the diseases we understand are much more specific than just 'these cells up and these cells down' - otherwise they would all be the same disease I guess. People talk about T regs because that is what grant money is given out for. They tend not to find out what we already know about a disease before saying it is all due to T regs.

 

[wastwater]

Do these t regs damp down the immune system and what if you were born with a fault there.
I was looking at the FOX gene family are they implicated in MS too FOXP3