CD4+ T cells acting independently of antibody contribute to protective immunity to Plasmodium chabaudi infection after apical membrane antigen 1 immunization.

摘要: Apical membrane Ag 1 (AMA1) is a leading malaria vaccine candidate. Homologues of AMA1 can induce protection in mice and monkeys, but the mechanism immunity not understood. Mice immunized with refolded, recombinant, Plasmodium chabaudi fragment (AMA1B) withstand subsequent challenge P. adami . Here we show that CD4 + T cell depletion, γδ cause significant drop antiparasite either normal or B KO mice. In mice, this loss accompanied by decline Ab levels. These observations indicate role for AMA1-specific Ab-independent cell-mediated immunity. However, cell-depleted temporary. Furthermore, cannot survive infection, demonstrating absolute importance cells, presumably Ab, AMA1-induced cells specific cryptic conserved epitope on adoptively transfer to athymic ( nu/nu ) level which enhanced cotransfer rabbit anti-AMA1-specific antisera. Recipients antisera alone do survive. Some protected recipients plus develop their own AMA 1-specific response, suggesting CMI protect data are first demonstrate specificity any protective response have important implications developing vaccine.