Passive immunity against infection with Trypanosoma brucei subsp. brucei in mice is conveyed by an antibody blocking the ligand-binding extracellular domain 1 (ed1) of the C2 receptor CRIT (47.20)

Abstract

Abstract Anti-CRIT-ed1 (recognising the first extracellular domain of CRIT) was passively transferred into mice which were subsequently challenged with 500 trypomastigotes of T. brucei subsp. brucei. At a peak of infection, eight days after challenge infection, mice that had received 0.5 mg anti-CRIT-ed1 (ascites) had significantly reduced levels of parasitaemia compared to control mice. This inhibiton was also found to be dose-dependent. As passive transfer of anti-CRIT-ed2, the antibody recognising the second extracellular domain did not reduce parasitaemia, the protection was deemed specific. The protection afforded by passive transfer of anti-CRIT-ed1 also delayed mortality. To exclude the possibility that the reduction in parasitaemia was due to intact IgG inducing complement-mediated lysis of trypomastigotes we found that whereas anti-CRIT-ed1 was unable to induce complement-mediated lysis of cultured trypomastigotes, the sera from T. brucei subsp brucei-infected mice induced lysis.