Hello, all!
Could anybody help me to elucidate the role of TGFbeta?
I know that Treg and Ti use it to downregulate the responce to antigens. But this cytokine releases into the environment, where many different T cells exist. Does it always suggests that TGFbeta mediated suppression is nonspecific and acts as a simple downregulator of the total Teff cells activity.
Or some degree of specificity nethertheless exists?

Hi
I am not so mfamilier with T cells but as I can TGFbeta has got some specificity towards Treg .
I found an article that maybe would be somewhat of help for you
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed
Guy

Thank you for your interest! It`s great that there is a place in the net where one can comunicate with other scientists!
...But the reference does not work..
Could you please type the author and the tittle?

The link didnt work for me
Here is another link
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15331781&query_hl=7&itool=pubmed_docsum

Hi Mischa,
happy that we can help you.
Tell your fellow scientist about this site. The more scientist will be members we will have more brians and the ability to answer more question much quicker.
Please, by kind and fill in "my bench space"

Here is the data you asked for :
Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14663-9. Epub 2004 Aug 26.

Dual effect of CD4+CD25+ regulatory T cells in neurodegeneration: a dialogue with microglia.

Kipnis J, Avidan H, Caspi RR, Schwartz M.

Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel.



Autoimmune CD4(+) T cells can mediate the ability to withstand neurodegenerative conditions. Here we show that the ability to spontaneously manifest a T cell-dependent protective response is restricted by naturally occurring CD4(+)CD25(+) regulatory T cells (Treg); depletion of Treg was beneficial in two mouse strains (C57BL/6J and BALB/c/OLA) differing in their spontaneous T cell-dependent ability to withstand the consequences of optic nerve injury. Passive transfer of exogenous Treg was destructive in BALB/c/OLA mice (which can spontaneously manifest a T cell-dependent protective anti-self response to injury) but beneficial in C57BL/6J mice (which have only limited ability to manifest such a response). This dichotomy was resolved by the finding that, in severe combined immunodeficient mice, a beneficial effect is obtained by passive transfer of either Treg-free CD4(+) T cells (Teff) or Treg alone, indicating that neuroprotection can be achieved by either Treg or Teff in the absence of the other. We attribute these disparate effects of Treg to their differential interaction (in part via IL-10 and transforming growth factor beta) with local innate immune cells (microglia) in the presence and in the absence of effector T cells. Activation of microglia by pro- and antiinflammatory cytokines in suitably controlled amounts might trigger different signal transduction pathways, each of which induces a neuroprotective microglial phenotype. These results suggest that, under neurodegenerative conditions, the effects of Treg, and possibly also of other regulatory T cells, might not be uniform, and that their expression in different individuals might be genetically determined. Therefore, therapeutic intervention based on induction of regulatory T cells might have limitations.
PMID: 15331781 [PubMed - indexed for MEDLINE]

>Tell your fellow scientist about this site.

OK!

>Please, by kind and fill in "my bench space"

I`ve got some trouble trying to change the settings... There is no "Change" or "Update" option in "my bench space".

The article have just been successfully downloaded... I`ll continue the discussion after reading...

Thanks COHscientist
And I will be looking forward for your reply Mischa
Guy

TGF-beta has an incredibly complex role, mediating a large number of cellular events, and its effects are highly dependent on what other processes are involved - for example TGF-beta's role in cancer can either be growth promoting or growth inhibitory, depending on when/where/how it is produced.

In other words, this is going to be a hard topic to sum up in one brief response.