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American Journal of Pathology, Vol 127, 335-341, Copyright © 1987 by American Society for Investigative Pathology

REGULAR ARTICLES

Coxsackievirus B3-induced myocarditis. Autoimmunity is L3T4+ T helper cell and IL-2 independent in BALB/c mice

M Estrin and SA Huber

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.


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S. Mikami, S. Kawashima, K. Kanazawa, K.-i. Hirata, H. Hotta, Y. Hayashi, H. Itoh, and M. Yokoyama
Low-Dose N{omega}-Nitro-L-Arginine Methyl Ester Treatment Improves Survival Rate and Decreases Myocardial Injury in a Murine Model of Viral Myocarditis Induced by Coxsackievirus B3
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Copyright © 1987 by the American Society for Investigative Pathology.