The disease now known as adjuvant arthritis of rats was discovered by Stoerk and coworkers (1) and by Pearson (2) independently. It is a disease of laboratory rats only. If an emulsion of mycobacteria (Cory- nebacterium and Nocardia organisms are also suitable) in light mineral oil is injected into the tail or a hind foot, generalized polyarthritis will occur, with peak activity at about 10 days (3). Pearson reviewed the various animal models of rheumatoid arthritis and concluded that adjuvant arthritis had a number of suitable features, although certain characteristics were different from the human disease (4). For instance, in adjuvant arthritis antigen-antibody complexes are not demonstrable and the serum complement level remains normal. Conversely, there is strong evidence for cellular mediation of both adjuvant disease and rheumatoid arthritis. Adjuvant arthritis may be transferred by injecting normal rats with thoracic duct lymphocytes from diseased animals or cell suspensions from lymph nodes or spleen. Only the cells, not the lymph itself, can transfer the disease (5). Previously, we found that antibody production, delayed hypersensitivity to dinitrochlorobenzene (DNCB), the rejection of skin allografts, and the development of adjuvant arthritis are all impaired in animals that have under-From the