Rheumatoid arthritis and seronegative spondyloarthropathies are rheuma
tologic diseases that likely are caused by inflammatory reactions occu
rring in genetically predisposed individuals mounting an immune respon
se to an antigen, Understanding the immunopathology of these diseases
provides insight into their etiology, pathogenesis, and a rationale fo
r therapies targeting immune component interactions, Although the anti
gen in rheumatoid arthritis is not known, several bacterial antigens h
ave been associated with seronegative spondyloarthropathies, These ant
igens result in an interaction between human leukocyte antigen-B27 res
tricted CD8 positive T lymphocytes and the antigen presenting cell, pr
oducing an inflammatory response, Rheumatoid factors are autoantibodie
s directed against the fragment crystallizable portion of the immunogl
obulin G. Rheumatoid factor immunoglobulin G immune complexes contribu
te to the inflammatory events in the rheumatoid joint, and may play an
important role in antigen presentation, A novel antigen capture enzym
e linked immunosorbent assay was developed that mimicked B cell surfac
e expressed rheumatoid factor, Conversely, a direct binding enzyme lin
ked immunosorbent assay mimicked secreted rheumatoid factor, Compariso
n of rheumatoid binding enzyme linked immunosorbent assays showed that
the physical state of rheumatoid factor can affect binding characteri
stics. The state of glycosylation of immunoglobulin G may contribute t
o its antigenic structure, These physical characteristics may be impor
tant in rheumatoid factor's pathogenic role in rheumatoid arthritis.