Vitiligo and non-self
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
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
Hope this helps.
(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.
> 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.
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