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PDBsum entry 2wbj
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Immune system
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PDB id
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2wbj
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Contents |
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178 a.a.
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179 a.a.
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193 a.a.
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270 a.a.
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188 a.a.
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References listed in PDB file
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Key reference
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Title
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T cell-Mediated autoimmune disease due to low-Affinity crossreactivity to common microbial peptides.
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Authors
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M.Harkiolaki,
S.L.Holmes,
P.Svendsen,
J.W.Gregersen,
L.T.Jensen,
R.Mcmahon,
M.A.Friese,
G.Van boxel,
R.Etzensperger,
J.S.Tzartos,
K.Kranc,
S.Sainsbury,
K.Harlos,
E.D.Mellins,
J.Palace,
M.M.Esiri,
P.A.Van der merwe,
E.Y.Jones,
L.Fugger.
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Ref.
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Immunity, 2009,
30,
348-357.
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PubMed id
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Abstract
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Environmental factors account for 75% of the risk of developing multiple
sclerosis (MS). Numerous infections have been suspected as environmental disease
triggers, but none of them has consistently been incriminated, and it is unclear
how so many different infections may play a role. We show that a microbial
peptide, common to several major classes of bacteria, can induce MS-like disease
in humanized mice by crossreacting with a T cell receptor (TCR) that also
recognizes a peptide from myelin basic protein, a candidate MS autoantigen.
Structural analysis demonstrates this crossreactivity is due to structural
mimicry of a binding hotspot shared by self and microbial antigens, rather than
to degenerate TCR recognition. Biophysical studies reveal that the autoreactive
TCR binding affinity is markedly lower for the microbial (mimicry) peptide than
for the autoantigenic peptide. Thus, these data suggest a possible explanation
for the difficulty in incriminating individual infections in the development of
MS.
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