Why the study?
Does anti-CD2 monoclonal antibody OX34 prevent the induction of experimental autoimmune myocarditis in Lewis rats?
Does anti-CD2 monoclonal antibody OX34 prevent the induction of experimental autoimmune myocarditis in Lewis rats?
Anti-CD2 monoclonal antibody OX34 completely prevents experimental autoimmune myocarditis when administered during the induction phase, likely via T cell depletion and anergy.
Does not support clinical use of anti-CD2 antibodies; leaves open translation of OX34-like strategies to human myocarditis.
We investigated the effect of a monoclonal antibody against CD2 molecules (OX34) in preventing the induction of experimental autoimmune myocarditis (EAM) induced by immunizing Lewis rats with cardiac myosin. Administration of OX34 before immunization, on Days -6, -4, -2 and 0, completely prevented EAM. On the other hand, treatment with OX34 just before the appearance of myocardial lesions, on Days 9, 11, 13 and 15, had only a partial effect in preventing the disease. Flow cytometric analysis of lymph node cells showed that CD3+ T cells were immediately depleted with the administration of OX34 but had largely recovered on Day 21. Lymph node cells in OX34-treated rats had no proliferative responses to cardiac myosin-rod, but the proliferation was restored when recombinant IL-2 was added. Ultimate production of the anti-myosin antibody was not inhibited by the treatment with OX34. These results suggest that the prevention of EAM by administering the anti-CD2 monoclonal antibody OX34 resulted from T cell depletion during the induction phase, and might in addition result from T cell anergy of Th1, but not Th2 cells.
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Inomata et al. (2000) studied this question.
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