Autoimmunity provoked by infection: how good is the case for T cell epitope mimicry?

[Guest guest]

Art Doherty posted this to the sci-med-diseases-lyme newsgroup. I didn't

see it posted here, hope I didn't miss it and this is duplicate.

From the NIH NLM MEDLINE database:

Nat Immunol 2001 Sep;2(9):797-801

Autoimmunity provoked by infection: how good is the case for T

cell epitope mimicry?

Benoist C, Mathis D.

Section on Immunology and Immunogenetics, Joslin Diabetes Center,

Department of Medicine, Brigham and Women's Hospital, Harvard Medical

School, One Joslin Place, Boston, MA, USA.

Autoimmune diseases remain one of the mysteries that perplex

immunologists. What makes the immune system, which has evolved to

protect an organism from foreign invaders, turn on the organism itself?

A popular answer to this question involves the lymphoid network's

primordial function: autoimmunity is a by-product of the immune

response to microbial infection. For decades there have been tantalizing

associations between infectious agents and autoimmunity: beta-hemolytic

streptococci and rheumatic fever; B3 sackieviruses and myocarditis;

Trypanosoma cruzi and Chagas' disease; diverse viruses and multiple

sclerosis; Borrelia burgdorfii [sic - of course, should be " burgdorferi]

and Lyme arthritis; and B4 sackievirus, cytomegalovirus or rubella

and type 1 diabetes, to name the most frequently cited examples. In

addition, animal models have provided direct evidence that infection

with a particular microbe can incite a particular autoimmune disease.

Nonetheless, many of the associations appear less than convincing and,

even for those that seem to be on solid footing, there is no real

understanding of the underlying mechanism(s).

PMID: 11526389 [PubMed - in process]

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list

_uids=11526389 & dopt=Abstract

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