The term reactive arthritis (ReA) was first used in 1969 to describe sterile joint disease that follows infection elsewhere in the body. This is an attempt to explain the immunological basis of this disease, give a rationale for the presence of a single bacterial antigen in the involved joints, explain why the class I MHC molecule HLA-B27 is necessary and to suggest possible therapy. This paper proposes an anti-idiotypic (anti-id) model for this disease where a bacterial lipopolysaccharide (LPS) epitope is recognized by idiotypic (Id) T cell receptors and antibody Fab immune recognition surfaces (IRS) which have the immunologic appearance of an antigen on the synovial surface. These Id immune effectors utilize an HLA-B27 molecule to present their IRS on their surface, which results in an anti-id response that can also target the synovial antigen. The anti-id IRS have the immunologic appearance of LPS and their detection in the arthritic joint falsely suggests the presence of bacterial LPS. Evidence is presented which supports this reactive arthritis model in which there is a synovial antigen that is attacked by an anti-id response against the LPS of arthritogenic bacteria. Therapeutic vaccination is supported by this hypothesis.
Copyright 2000 Harcourt Publishers Ltd.