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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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* Residue conservation analysis
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PDB id:
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Immune system
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Title:
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Tcr complex
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Structure:
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Hla class ii histocompatibility antigen, dr alpha chain. Chain: a, e. Fragment: mhc class ii, residues 26-218. Synonym: mhc class ii antigen dra. Engineered: yes. Hla class ii histocompatibility antigen, drb1-15 beta chain. Chain: b, f. Fragment: mhc class ii, residues 29-227.
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Source:
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Homo sapiens. Human. Organism_taxid: 9606. Expressed in: drosophila melanogaster. Expression_system_taxid: 7227. Expression_system_cell_line: s2 cells. Expressed in: escherichia coli. Expression_system_taxid: 469008. Other_details: patient derived sequence.
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Resolution:
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3.00Å
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R-factor:
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0.249
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R-free:
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0.288
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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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Key ref:
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M.Harkiolaki
et al.
(2009).
T cell-mediated autoimmune disease due to low-affinity crossreactivity to common microbial peptides.
Immunity,
30,
348-357.
PubMed id:
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Date:
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02-Mar-09
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Release date:
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07-Apr-09
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PROCHECK
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Headers
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References
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P01903
(DRA_HUMAN) -
HLA class II histocompatibility antigen, DR alpha chain from Homo sapiens
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Seq:
Struc:
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254 a.a.
178 a.a.
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P01911
(2B1F_HUMAN) -
HLA class II histocompatibility antigen, DRB1 beta chain from Homo sapiens
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Seq:
Struc:
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266 a.a.
179 a.a.
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No UniProt id for this chain
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Immunity
30:348-357
(2009)
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PubMed id:
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T cell-mediated autoimmune disease due to low-affinity crossreactivity to common microbial peptides.
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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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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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Literature references that cite this PDB file's key reference
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PubMed id
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Reference
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C.Kurts,
B.W.Robinson,
and
P.A.Knolle
(2010).
Cross-priming in health and disease.
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Nat Rev Immunol,
10,
403-414.
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L.Fugger,
M.A.Friese,
and
J.I.Bell
(2009).
From genes to function: the next challenge to understanding multiple sclerosis.
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Nat Rev Immunol,
9,
408-417.
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The most recent references are shown first.
Citation data come partly from CiteXplore and partly
from an automated harvesting procedure. Note that this is likely to be
only a partial list as not all journals are covered by
either method. However, we are continually building up the citation data
so more and more references will be included with time.
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