heexposure of rabbits to Mycoplasma arthntidis predisposed them to subsequent development of chronic inflammation in knee joints challenged with nonviable A4 arthritidis antigens. Rabbits sensitized by hyperimmunization developed a more severe arthritis than those sensitized by infection. Unsensitized rabbits responded minimally to intraarticular injection of nonviable organisms. These results suggested that an immune response to a persisting mycoplasmal antigen might be capable of sustaining chronic inflammation in rabbits with arthritis induced by viable M arthntidis.We have shown that Mycoplasma arthritidis, which causes arthritis in rats (1,2) and mice (3,4), also induces arthritis in rabbits after intraarticular injection (5-7). Although the rabbit disease can last as long as 1 year, neither viable organisms nor mycoplasmal antigens appear to persist in joint tissues longer than a few weeks. Therefore, the mechanisms of chronicity are unclear. Throughout both acute and chronic stages, we detected heavy lymphocyte and plasma cell infiltration of synovial tissue through 52 weeks, as well as numerous granular deposits that contained IgG and C3 in synovium and articular cartilage. In addition, a cellmediated immune response (unpublished) and an intense local antibody response to M arthritidis antigens persisted for at least 31 and 52 weeks, respectively., These observations suggested that the chronic phase was at least partly mediated by immunologic mechanisms.We previously suggested (7) that the pathogenesis of M arthritidis-induced arthritis of rabbits might be similar to that proposed by Cooke et a1 for experimental antigen-induced arthritis (8-10). Chronic antigen-induced arthritis results when an animal that has been preimmunized with an antigen in complete Freund's adjuvant is challenged intraarticularly with the same antigen in an aqueous medium (1 I). Cooke et al demonstrated the localization of the injected antigen in the form of immune complexes in articular cartilage, meniscus, and ligaments and suggested that antigen that persists in these tissues provided the immunologic stimulus for chronic joint inflammation (9). The pattern of immune complex deposition that we saw in the articular cartilage of M arthritidis-injected rabbits (7) was very similar to that described by these investigators. However, we were unable to detect mycoplasmal antigens in these complexes by immunofluorescence (6).To show that an immune response to mycoplasma1 antigens might indeed contribute to the persistence of chronic inflammatory arthritis, we induced arthritis in preimmunized rabbits by intraarticular challenge with nonviable mycoplasmal antigens. We have also shown that intraarticular challenge with nonviable antigens of rabbits previously infected with viable M arthritidis, but not otherwise presensitized,