FAILURE OF TREATMENT WITH INTERLEUKIN-2 RECEPTOR-SPECIFIC MONOCLONAL-ANTIBODY IN ACUTE COXSACKIEVIRUS B3 MYOCARDITIS IN MICE

T cell activation is assumed to play a crucial role in many viral infe ctions. An important marker for the activation of T cells is the inter leukin-receptor (IL-2R); resting T lymphocytes do not bear detectable amounts of IL-2R. AMT13, a rat monoclonal antibody against mouse IL-2R , inhibits interleukin-2-dependent cell growth both in vitro and in vi vo. Therefore, to clarify the effects of anti-IL-2R antibody treatment upon coxsackievirus B3 (CB3)-infected C3H/He mice, AMT13, 1 mu g/mous e per day, was administered, subcutaneously, starting on day 0 (group 2) in experiment I or on day 7 (group 4) in Experiment II for 7 days, respectively. Groups 1 and 3 were examined as infected controls. In bo th experiments, there was no significant difference in mortality or in the severity of myocarditis between the treated and the untreated gro ups. Also, myocardial CB3 titers on day 7 did not differ significantly between groups 1 and 2. In addition, the distribution of activated T cell subsets in the inflamed myocardium was not changed by the treatme nt, and the paucity of myocardial IL-2R-positive cells was confirmed i n all groups. Effects of the antibody treatment were confirmed by a de crease in delayed type hypersensitivity. Although some reports have sh own that anti-IL-2R antibody has been successfully applied to ameliora te acute renal graft-versus-host disease, to enhance survival of skin allografts, and to suppress diabetic insulitis, it did not exert a ben eficial effect on acute CB3 myocarditis in mice.