ROLE OF T-LYMPHOCYTES IN ADJUVANT ARTHRITIS .2. DIFFERENT SUB-POPULATIONS OF T-LYMPHOCYTES FUNCTIONING IN DEVELOPMENT OF DISEASE

Abstract

The effects of treatments with cyclophosphamide (CY), hydrocortisone [HC] and anti-thymocyte sera (ATS) on the development of adjuvant arthritis (AA) were examined in WKA rats inoculated with wax D to induce AA. A single injection of 25-50 mg/kg of CY given 2-3 days before wax D inoculation caused severe arthritis with high incidence. Larger doses of CY were less efficient. The enhancing effect of CY pretreatment was abolished by passively transferred normal syngeneic thymocytes 1 day before wax D inoculation, but not by thymocytes that were treated with ATS and guinea pig C [complement]. This enhancing effect of CY pretreatment was probably caused by selective depletion of suppressor T [thymus-derived] lymphocytes. Pretreatment with 12.5 mg of HC also caused severe arthritis. This enhancing effect of HC could also be due to the elimination of those suppressor cells. In vivo pretreatment with ATS showed striking inhibition on the development of AA, suggesting that ATS could eliminate T lymphocytes that were responsible for eliciting this disease. Thus it appears that at least 2 T cell subpopulations are involved in the development of AA; one is an ATS-sensitive T2 subpopulation that is effective for induction of AA and the other is a T1 subpopulation that regulates this disease process.