UC Merced

Parasitic disease is a global health burden. Current and historical efforts to eradicate parasitic disease rely heavily on vector control and mass drug administration campaigns rather than vaccine induced immunity due in large part to effective parasite immune evasion. Toxoplasma gondii is an intracellular protozoal parasite estimated to infect up to a third of the world’s population, is the second leading cause of food-borne disease in the United States and demonstrates evasion of vaccine induced immunity (CDC, 2017). Previous work done by our lab suggest a crucial role for B-1 cells for the control and clearance of highly virulent T. gondii strains. A genetic link between Nfkbid and the resistant murine phenotype prompted our endeavor to analyze antibody reactivity to T. gondii. We used serum antibody to probe T. gondii protein via western blot and found 1) A/J and C57BL/6J serum IgM and total IgG antibody target the same proteins below 50kDa which are likely known GPI anchored proteins, 2) B-1 cell deficient Nfkbid null C57BL/6J mice lose 87% serum IgM reactivity and 91% total IgG reactivity when compared to wild type C57BL/6J mice, 3) A/J and C57BL/6J antibody reactivity to T. gondii protein relies heavily on the presence of the lipid moiety of the GPI anchor and 4) A/J mice to produce more antibody overall than C57BL/6J mice. These findings contribute to our growing body of work which correlates resistance to T. gondii infection with enhanced antibody production to antigens likely targeted by B-1 cells. Resolution of the contribution of this protective antibody response may provide novel insight for the development of a completely protective and long-lasting vaccine against parasite.