IMMUNOLOGY OF REACTIVE ARTHRITIDES

Reactive arthritis (ReA) and Lyme arthritis together comprise a pair o f chronic inflammatory diseases of the joints. Although differing in d etail, these relatively rare diseases are related in their immunopatho logy to the much commoner rheumatoid arthritis (RA), for which they se rve as both model and control. The trigger for rheumatoid arthritis is unknown, but for these rarer diseases triggering occurs by certain we ll-defined bacterial infections. Arthritis is an uncommon outcome of t hese infections, for reasons unknown, and the development of chronic, as distinct from brief, arthritis is even rarer; again, the reasons ar e unknown. Not only does knowing the trigger greatly assist us in unde rstanding these diseases, so also does knowing the contrasting pattern of Th1 versus Th2 cytokines observed in RA and ReA. ReA and Lyme arth ritis are here considered in the wider setting of infections where chr onic morbidity arises first from hypersensitivity, and perhaps finally from autoimmunity, such as occurs in some of the major tropical disea ses. The immunology of ReA and Lyme disease is surveyed in detail, con centrating on T cells and including an update on the Lyme vaccine(s). Additional sections deal with the enigma of HLA B27, with epidemiologi cal findings relevant to the chronicity of ReA and to the need for enl arged prospective studies of ReA in the setting of a developing countr y.