CORTICOSTEROID IMMUNOSUPPRESSION AND MONOCLONAL ANTIBODY-MEDIATED CD5(-LYMPHOCYTE DEPLETION IN NORMAL AND EQUINE INFECTIOUS-ANEMIA VIRUS-CARRIER HORSES() T)

The immune control of chronic equine infectious anaemia (EIA) lentivir al infection was investigated by specifically depleting CD5(+) T lymph ocytes in vivo with monoclonal antibody (MAb) or by immunosuppression with corticosteroids. MAb was given at 25 to 50 mg/day intravenously f or 11 days. Murine IgG1 anti-equine CD2 MAb (n = 2 horses) or IgG1 (n = 2) and IgG2a control MAb (n = 2 normal; 2 EIA-infected) did not depl ete CD2(+) T lymphocytes in horses. Horses given murine IgG2a anti-CDS MAb HB19A (n = 4 normal; 5 EIA-infected) had depletion of peripheral blood CD5(+) T lymphocytes during treatment. These horses, however, ma intained a residual population of CD2(+) T lymphocytes [15 (+/- 3)% of pretreatment numbers] that did not express CD5 but expressed either C D4 or CD8. These antigenically modulated CD5(-) T lymphocytes responde d normally in vivo to intradermal inoculation with phytohaemagglutinin and in vitro to allogeneic leukocyte stimulation in one-way mixed lym phocyte reactions. EIA virus-infected horses (n=5) did not develop rec rudescent viraemia or disease following in vivo CD5(+) T lymphocyte de pletion. Immunosuppression of EIA virus-infected horses with corticost eroids (1 mg/kg body weight/day, intravenously for 9 days) resulted in detectable recrudescent EIA viraemia in 6/11 horses (55%) and recrude scent disease in 9/11 horses (82%). Normal horses (n = 3) treated with corticosteroids developed no clinical disease. These results demonstr ate that the use of murine IgG2a MAbs to appropriate equine lymphocyte antigens will facilitate in vivo investigation of the role of T lymph ocyte subpopulations in the control of EIA or other important equine d iseases.