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PDBsum entry 2wbj

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protein ligands Protein-protein interface(s) links
Immune system PDB id
2wbj
Jmol PyMol
Contents
Protein chains
178 a.a. *
179 a.a. *
193 a.a. *
270 a.a. *
188 a.a. *
Ligands
NAG ×4
SO4 ×3
NAG-NAG-BMA-MAN-
MAN
* Residue conservation analysis
PDB id:
2wbj
Name: Immune system
Title: Tcr complex
Structure: Hla class ii histocompatibility antigen, dr alpha 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 chain. Chain: b, f. Fragment: mhc class ii, residues 29-227.
Source: 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.
Resolution:
3.00Å     R-factor:   0.249     R-free:   0.287
Authors: 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 S.Sainsbury,K.Harlos,E.D.Mellins,J.Palace,M.M.Esiri, P.A.Van Der Merwe,E.Y.Jones,L.Fugger
Key ref: 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: 19303388
Date:
02-Mar-09     Release date:   07-Apr-09    
PROCHECK
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 Headers
 References

Protein chains
Pfam   ArchSchema ?
P01903  (DRA_HUMAN) -  HLA class II histocompatibility antigen, DR alpha chain
Seq:
Struc:
254 a.a.
178 a.a.
Protein chain
Pfam   ArchSchema ?
P01911  (2B1F_HUMAN) -  HLA class II histocompatibility antigen, DRB1-15 beta chain
Seq:
Struc:
266 a.a.
179 a.a.
Protein chains
No UniProt id for this chain
Struc: 193 a.a.
Protein chains
No UniProt id for this chain
Struc: 270 a.a.
Protein chain
Pfam   ArchSchema ?
P01911  (2B1F_HUMAN) -  HLA class II histocompatibility antigen, DRB1-15 beta chain
Seq:
Struc:
266 a.a.
188 a.a.
Key:    PfamA domain  Secondary structure  CATH domain

 Gene Ontology (GO) functional annotation 
  GO annot!
  Cellular component     membrane   2 terms 
  Biological process     immune response   2 terms 

 

 
Immunity 30:348-357 (2009)
PubMed id: 19303388  
 
 
T cell-mediated autoimmune disease due to low-affinity crossreactivity to common microbial peptides.
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.
 
  ABSTRACT  
 
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.
 

Literature references that cite this PDB file's key reference

  PubMed id Reference
20498667 C.Kurts, B.W.Robinson, and P.A.Knolle (2010).
Cross-priming in health and disease.
  Nat Rev Immunol, 10, 403-414.  
19444306 L.Fugger, M.A.Friese, and J.I.Bell (2009).
From genes to function: the next challenge to understanding multiple sclerosis.
  Nat Rev Immunol, 9, 408-417.  
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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