HLA-B27 transgenic animal models suggest a role for CD4(+) T lymphocytes in
the pathogenesis of the spondyloarthropathies, and murine studies have rai
sed the possibility that unusual forms of B27 may be involved in disease. W
e demonstrate that CD4(+) T cells capable of recognizing B27 can be isolate
d from humans by coculture with the MHC class II-negative cell line T2 tran
sfected with B27. These CD4(+) T cells recognize a panel of B27-transfected
cell lines that are defective in Ag-processing pathways, but not the nontr
ansfected parental cell lines, in a CD4-dependent fashion. Inhibition of re
sponses by the MHC class I-specific mAb w6/32 and the B27 binding mAb ME1 i
mplicates 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 spondyloa
rthropathies, particularly if factors such as infection influence expressio
n of abnormal forms of B27.