The recognition of HLA-B27 by human CD4(+) T lymphocytes.
HLA-B27 transgenic animal models suggest a role for CD4(+) T lymphocytes in the pathogenesis of the spondyloarthropathies, and murine studies have raised the possibility that unusual forms of B27 may be involved in disease. We demonstrate that CD4(+) T cells capable of recognizing B27 can be isolated from humans by coculture with the MHC class II-negative cell line T2 transfected with B27. These CD4(+) T cells recognize a panel of B27-transfected cell lines that are defective in Ag-processing pathways, but not the nontransfected parental cell lines, in a CD4-dependent fashion. Inhibition of responses by the MHC class I-specific mAb w6/32 and the B27 binding mAb ME1 implicates the recognition of a form of B27 recognized by both of these Abs. We suggest that B27-reactive CD4(+) T cells may be pathogenic in spondyloarthropathies, particularly if factors such as infection influence expression of abnormal forms of B27.
Boyle
L H
LH
University of Cambridge School of Clinical Medicine, Department of Medicine, Cambridge, United Kingdom.
Goodall
J C
JC
Opat
S S
SS
Gaston
J S
JS
D000818:Animals; D000911:Antibodies, Monoclonal; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D002460:Cell Line; D002472:Cell Transformation, Viral; D018920:Coculture Techniques; D015796:HLA-B27 Antigen / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D004854:Herpesvirus 4, Human; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D025242:Spondylarthropathies / Q000209:etiology / Q000235:genetics / Q000276:immunology; D013167:Spondylitis, Ankylosing / Q000276:immunology; D014162:Transfection
D000911:Antibodies, Monoclonal; D015796:HLA-B27 Antigen