Anti-CD2 monoclonal antibodies prevent the induction of experimental autoimmune myocarditis

We investigated the effect of a monoclonal antibody against CD2 molecules ( OX34) in preventing the induction of experimental autoimmune myocarditis (E AM) induced by immunizing Lewis rats with cardiac myosin. Administration of OX34 before immunization, on Days -6, -4, -2 and 0, completely prevented E AM. On the other hand, treatment with OX34 just before the appearance of my ocardial lesions, on Days 9, 11, 13 and 15, had only a partial effect in pr eventing the disease. Flow cytometric analysis of lymph node cells showed t hat CD3(+) T cells were immediately depleted with the administration of OX3 4 but had largely recovered on Day 21. Lymph node cells in OX34-treated rat s had no proliferative responses to cardiac myosin-rod, but the proliferati on was restored when recombinant IL-2 was added. Ultimate production of the anti-myosin antibody was not inhibited by the treatment with OX34. These r esults suggest that the prevention of EAM by administering the anti-CD2 mon oclonal antibody OX34 resulted from T cell depletion during the induction p hase, and might in addition result from T cell anergy of Th1, but not Th2 c ells.