Journal
JOURNAL OF AUTOIMMUNITY
Volume 29, Issue 4, Pages 262-271Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jaut.2007.07.014
Keywords
autoimmunity; T cell receptor; molecular mimicry; multiple sclerosis; immune tolerance
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Funding
- Medical Research Council [G117/515] Funding Source: researchfish
- MRC [G117/515] Funding Source: UKRI
- Medical Research Council [G117/515] Funding Source: Medline
- Multiple Sclerosis Society [813] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
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Extensive cross-reactivity in T cell receptor (TCR) recognition of peptide-MHC (pMHC) complexes seems to be essential to give sufficient immune surveillance against invading pathogens. This carries with it an inherent risk that T cells activated during a response to clear an infection can, perhaps years later, respond to a self pMHC of sufficient similarity. This lies at the heart of the molecular mimicry theory. Here we discuss our studies on the disease-causing potential of altered peptide ligands (APL) based on the sequence of a single autoantigenic epitope, the Ac1-9 peptide of myelin basic protein that induces experimental autoimmune encephalomyelitis in mice. These show that the window of similarity to self for induction of disease by cross-reactive non-self peptides is actually quite restricted. We show that each of the three pillars of immune tolerance (death, anergy/adaptation and regulation) has a role in limiting the risk of molecular mimicry by maintaining a threshold for harm. (c) 2007 Elsevier Ltd. All rights reserved.
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