title: Corticosteroid immunosuppression and monoclonal antibody-mediated CD5+ T lymphocyte depletion in normal and equine infectious anaemia virus-carrier horses.
abstract: The immune control of chronic equine infectious anaemia (EIA) lentiviral infection was investigated by specifically depleting CD5+ T lymphocytes in vivo with monoclonal antibody (MAb) or by immunosuppression with corticosteroids. MAb was given at 25 to 50 mg/day intravenously for 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 deplete CD2+ T lymphocytes in horses. Horses given murine IgG2a anti-CD5 MAb HB19A (n = 4 normal; 5 EIA-infected) had depletion of peripheral blood CD5+ T lymphocytes during treatment. These horses, however, maintained a residual population of CD2+ T lymphocytes [15 (+/- 3)% of pretreatment numbers] that did not express CD5 but expressed either CD4 or CD8. These antigenically modulated CD5- T lymphocytes responded normally in vivo to intradermal inoculation with phytohaemagglutinin and in vitro to allogeneic leukocyte stimulation in one-way mixed lymphocyte reactions. EIA virus-infected horses (n = 5) did not develop recrudescent viraemia or disease following in vivo CD5+ T lymphocyte depletion. Immunosuppression of EIA virus-infected horses with corticosteroids (1 mg/kg body weight/day, intravenously for 9 days) resulted in detectable recrudescent EIA viraemia in 6/11 horses (55%) and recrudescent disease in 9/11 horses (82%). Normal horses (n = 3) treated with corticosteroids developed no clinical disease. These results demonstrate that the use of murine IgG2a MAbs to appropriate equine lymphocyte antigens will facilitate in vivo investigation of the role of T lymphocyte subpopulations in the control of EIA or other important equine diseases.
authors.affiliation: Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman 99164-7040.
authors.forename: D B
authors.initials: DB
authors.lastname: Tumas
authors.forename: M T
authors.initials: MT
authors.lastname: Hines
authors.forename: L E
authors.initials: LE
authors.lastname: Perryman
authors.forename: W C
authors.initials: WC
authors.lastname: Davis
authors.forename: T C
authors.initials: TC
authors.lastname: McGuire
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D015703:Antigens, CD / Q000276:immunology*; D001773:Blood Cells / Q000276:immunology; D018956:CD5 Antigens; D002353:Carrier State / Q000276:immunology*; D002908:Chronic Disease; D003167:Complement Activation; D003907:Dexamethasone / Q000494:pharmacology; D004859:Equine Infectious Anemia / Q000209:etiology / Q000276:immunology* / Q000517:prevention & control; D005434:Flow Cytometry; D006736:Horses; D007074:Immunoglobulin G / Q000494:pharmacology; D007165:Immunosuppression Therapy; D008212:Lymphocyte Depletion; D011817:Rabbits; D012008:Recurrence; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014766:Viremia
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D018956:CD5 Antigens; D007074:Immunoglobulin G; D003907:Dexamethasone