Cellualr Subsets Involved in Protective Immunity to Babesiarodhaini Infection in BALB/c Mice

Protective immune responses and the functional role of spleen cells in mice infected with Babesia rodhaini were examined with an in vitro proliferation assay systems and by in vivo passive transfer of spleen cells to uninfected mice. Mice that resolved primary babesial infection after chemotherapy (Babesia immune mice) had transient and low parasitemia after challenge infection and high rates (75%) of survival. Babesia hyperimmune mice, by contrast, had no detectable parasitemia after challenge and 100% survival. Proliferative response of spleen cells to Babesia lysate antigen (BLA) were determined for mice from both groups. This proliferative response was inhibited by treatment of spleen cells with anti-T cell serum and monoclonal antibody (MAb) to Lyt l antigen. Spleen cells of hyperimmime mice produced larger amount of IL-2 production than those of immune mice. Transfer of spleen cells from immune mice to nonimmune mice provided protection against babesial infection and recipient mice had high titers of anti-babesial antibody. When these spleen cells were treated with anti-T cell serum or anti-mouse Ig serum, protection against challenge was abolished. By contrast, transfer of hyperimmune spleen cells was capable of protecting recipient mice. Treatment of hyperimmune spleen cells with antiserum to mouse Ig or MAb against Lyt 1 and Lyt 2 antigens did not interfere with their ability to protect recipient mice against infection, even though recipient mice had low levels of antibody production. These results indicate that humoral immune response is important in establishing protection after primary infections while the panicipation of Lyt 1+ cells and Lyt 2+ cells and other aspects of the cell-mediated immune response is important in controlling secondary infections