title: HLA-B27 and disease: a consequence of inadvertent antigen presentation?
abstract: The close association of HLA-B27 with arthritic conditions has led to the suggestion that these diseases are mediated by cytotoxic T lymphocytes that recognize self-peptides presented by HLA-B27 molecules. The further association with enteric bacterial infections suggests that bacterial antigens may prime the CTL that later crossreacts on self. Bacterial infections do not usually generate CTL responses. We speculate here that unusual properties of HLA-B27 molecules may predispose to such responses. Thus, HLA-B27-related disease may be an unfortunate consequence of the generation of a suitable, self-mimicking HLA-B27-binding peptide by certain bacteria, plus an unusual propensity for the HLA-B27 molecule to bind and present such peptides.
authors.affiliation: Department of Cell Biology, Stanford University Medical School, California.
authors.forename: R
authors.initials: R
authors.lastname: Benjamin
authors.forename: P
authors.initials: P
authors.lastname: Parham
mesh_terms: D001168:Arthritis / Q000276:immunology*; D015796:HLA-B27 Antigen / Q000032:analysis* / Q000276:immunology / Q000502:physiology; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006801:Humans; D010455:Peptides / Q000276:immunology / Q000378:metabolism; D013167:Spondylitis, Ankylosing / Q000276:immunology*
chemical_list: D015796:HLA-B27 Antigen; D000949:Histocompatibility Antigens Class II; D010455:Peptides