Coxsackievirus B3-induced myocarditis. Autoimmunity is L3T4+ T helper cell and IL-2 independent in BALB/c mice.
Male BALB/c mice inoculated with 6 X 10(4) plaque-forming units (pfu) coxsackievirus, group B, type 3 (CVB3), develop myocarditis within 7 days. Two cytolytic T lymphocyte (CTL) populations arise in infected animals. One population belongs to the Lyt 2+ T (cytolytic/suppressor) lymphocyte subset and reacts specifically with uninfected heart cells (autoreactive CTLs, ACTLs), whereas the other belongs to the L3T4+ T (helper) lymphocyte subset and reacts with infected targets (virus-specific CTLs, VSCTLs). Although both immune T lymphocyte populations can induce cardiac inflammation in vivo, ACTLs predominantly cause tissue injury. VSCTL generation can be inhibited by either anti-Tac (antibody to the interleukin 2 [IL-2] receptor) or anti-Iad but not by anti-IAk, indicating that this response is probably both IL-2-dependent and Class II (major histocompatibility complex [MHC] antigen restricted. ACTL generation is independent of IL-2, because neither anti-Tac or cyclosporin A inhibit this response.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte; D000954:Antigens, Surface / Q000276:immunology*; D001327:Autoimmune Diseases / Q000276:immunology*; D003384:Coxsackievirus Infections / Q000276:immunology*; D003524:Cyclosporins / Q000494:pharmacology; D029822:Enterovirus B, Human; D007376:Interleukin-2 / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7
D000911:Antibodies, Monoclonal; D000945:Antigens, Differentiation, T-Lymphocyte; D000954:Antigens, Surface; D003524:Cyclosporins; D007376:Interleukin-2; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7