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 Sch istosoma mansoni has been investigated in a mouse strain rendered gene tically B-cell deficient (the mu MT 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 excep t at 10 weeks of infection. In addition, analysis of the cytokine prof iles (IL-2, IL-4, IL-5 and IFN-gamma), investigated using RT-PCR, show ed that spleens of mu MT animals displayed a predominant Th1-like prof ile compared to control, B-cell-intact infected mice. This showed that B cells, either per se or through their secretions, are involved in t he in vivo generation and/or maximal expansion of Th2-type T lymphocyt es during the course of murine S. mansoni infection. Interestingly, th e data showed that B-cell-deficient mice display an increased hepatic fibrosis at 10 weeks postinfection (p.i.), whereas they behaved like i nfected controls, with regard to the other assessed parasitological pa rameters (e.g. worm burden estimation). This demonstrated that even if B lymphocytes are not essential for the development of the general im mune response towards S. mansoni in the mouse, they may nevertheless b e involved in the correct immunoregulation of the granulomatous reacti on around the eggs.