Infection of B-cell-deficient mice by the parasite Schistosoma mansoni: demonstration of the participation of B cells in granuloma modulation.

The contribution of B lymphocytes to immunity towards the parasite Schistosoma mansoni has been investigated in a mouse strain rendered genetically B-cell deficient (the muMT mouse). These studies demonstrated that T cells primed in vivo in B-cell-deficient mice proliferate less efficiently in vitro in response to parasite antigenic extracts except at 10 weeks of infection. In addition, analysis of the cytokine profiles (IL-2, IL-4, IL-5 and IFN-gamma), investigated using RT-PCR, showed that spleens of muMT animals displayed a predominant Th1-like profile compared to control, B-cell-intact infected mice. This showed that B cells, either per se or through their secretions, are involved in the in vivo generation and/or maximal expansion of Th2-type T lymphocytes during the course of murine S. mansoni infection. Interestingly, the data showed that B-cell-deficient mice display an increased hepatic fibrosis at 10 weeks postinfection (p.i.), whereas they behaved like infected controls, with regard to the other assessed parasitological parameters (e.g. worm burden estimation). This demonstrated that even if B lymphocytes are not essential for the development of the general immune response towards S. mansoni in the mouse, they may nevertheless be involved in the correct immunoregulation of the granulomatous reaction around the eggs.