Modulation of murine host‐versus‐graft disease by anti‐CD3 monoclonal antibody
BALB/c mice made tolerant to A/J alloantigens by neonatal injection of (A/J × BALB/c)FI spleen cells develop a host‐versus‐graft (HVG) disease due to the activation of donor B cells by a subset of host alloreactive helper T cells. We have investigated the effects of a single neonatal injection of the 145‐2C11 anti‐mouse CD3 monoclonal antibody (MoAb) on the establishment of allotolerancc and on the development of the immunopathological features of HVG disease. First, this treatment did not modify the specific anti‐donor cytotoxic T lymphocyte (CTL) unresponsiveness or the persistence of circulating immunoglobulins bearing donor allotype. Second, the hyper IgE, the hyper IgG 1 and the increased expression of Ia antigens on B cells found in untreated HVG mice were not observed after injection of the 145‐2C11 MoAb. Likewise, treated mice displayed lower levels of anti‐DNA IgG antibodies and less glomerular immune deposits as compared with untreated HVG mice. We conclude that the administration of the anti‐CD3 MoAb did not interfere with the induction of allotolerance but exerts a pronounced inhibitory effect on the associated immunopathological syndrome.