Vitiligo and non-self

Daniele Focosi mi at interhealth.info
Sun Mar 7 04:04:05 EST 2004


Skin trauma is likely to induce cell necrosis and escape of
intracellular proteins into the interstitial fluid. Heat-shock protein
have been shown to be highly potent danger signals for activation of
dendritic cells, the starting point of adaptive immune response : once
dendritic cells have been activated, they have the potential for
trigger an immune response to any protein found in the inflamed area.
With reference to the mentioned article
(http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14973051&dopt=Abstract),
it would be interesting to look for any form of autoimmune myositis in
the mice exposed to i.m. vaccination : if it would lack, we could
hypothetize muscle tissue is more resistant to necrosis than dermis
and it will agree with the fact that it is far more stable (less
self-renewable) than skin. For more details on danger theory see
http://xoomer.virgilio.it/medicine/dangertheory.html .
Hope this helps.

Daniele Focosi
(Molecular Immunology webmaster : http://www.mi.interhealth.info)

"Donald Forsdyke" <forsdyke at post.queensu.ca> wrote in message news:<d6c2c.2842$R37.2027 at read1.cgocable.net>...
> In organisms inwhich melanomas are being attacked by host T-lymphocytes,
> patches of pale skin sometimes appear ("vitiligo"). It seems that the
> T-lymphocytes are attacking not only the melanoma cells, but also the
> relatively uniformly distributed melanin-producing cells in the skin. This
> is consistent with the idea that normal self antigens (not specific tumor
> antigens) are the usual targets of cytotoxic T-lymphocytes.
> 
>      One explanation of vitiligo would be that specific host T-lymphocytes
> are at a very low concentration and the patches appear where a specific
> T-lymphocyte happens to encounter an appropriate antigen on a skin cell.
> However, a recent paper in Cancer Research by Lane et al. (February 15)
> presents evidence that the vitiligo is secondary to trauma. Thus, there may
> be an abundance of T-lymphocytes of a sufficient degree of specificity, but
> they only attack when some "not-self" (i.e. external) agent has inflicted
> trauma on the skin. Thus, the first event is triggering by not-self. This
> would provoke the upregulation of MHC-protein production and the
> presentation of peptides for T-cell recognition.
> 
> Cheers,
> Donald Forsdyke. Discussion Leader. Bionet.immunology
> 
> This message was sent to Bionet.immunology, but the newsgroup "could not be
> resolved" so it is being sent to the other group for which I am Discussion
> Leader, Bionet.journals.note. Hopefully, someone in the Bionet
> administration will "upregulate" Bionet.immunology so that it can be
> resolved in future.



More information about the Immuno mailing list