In infection with Schistosoma mansoni, B cells are required for T helper type 2 cell responses but not for granuloma formation.

The immune response and immunopathologic manifestations in schistosomiasis are largely dependent on Ag-specific CD4+ Th cells. In turn, the stimulatory/regulatory function of the Th cells is dependent on signals emanating from accessory cells. B cells are capable of functioning as accessory cells, and their role in experimental murine schistosomiasis was investigated by using mice with targeted mutations in the J(H) locus. This phenotype results in the absence of B cells and of Ab production. After 7.5- to 8-wk infections, mesenteric lymph node cells from the JHD B-less mice displayed lower proliferative responses to schistosomal egg Ag than did cells from infected control mice. Most importantly, compared with cells from controls, egg Ag-stimulated JHD lymph node cells produced significantly higher amounts of the Th1 response-associated cytokines IFN-gamma and IL-12, while their production of the Th2-type cytokines IL-4 and IL-10 was dramatically reduced or undetectable. Similarly, irradiated splenocytes from uninfected JHD mice, used as APC, elicited significantly stronger Th1 and weaker Th2 responses from egg Ag-specific CD4+ Th cells than splenocytes from control mice. Despite these sharply contrasting cytokine profiles, there were no significant differences either in the size and composition of the resulting egg granulomas or in the number of deposited eggs in the livers of infected JHD vs control mice. Taken together, the findings in the JHD mouse reflect an impairment in the ability to mount a Th2 response, which translates into a loss of the Th1 to Th2 switch characteristically seen in normal schistosome-infected mice. These results suggest that B cells promote Th2-type responses, and that typical granulomatous responses proceed in their absence.