IMMUNOLOGICAL RESPONSE OF MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II-DEFICIENT (A-BETA-DEGREES) MICE INFECTED BY THE PARASITE SCHISTOSOMA-MANSONI

We have characterized the immunological behaviour of major histocompit ibility complex (MHC) Class II. molecule-deficient (A beta degrees) mi ce after infection by Schistosoma mansoni. In A beta degrees mice, mor bidity developed dramatically 7 weeks after infection leading to death , despite the absence of an increase in parasite burden or of eggs tra pped in the liver. Histological examination of the liver revealed the absence of a classical granulomatous reaction. Antibodies were produce d only against schistosomulum antigens. Specific antibodies against ad ult worm (SWAP) or egg antigen (SEA) were not detected. Cytokine produ ction (IFN-gamma and IL-4) was absent after in vitro restimulation of splenic cells from infected A beta degrees mice with parasite antigens . Adoptive transfer of primed splenic cells (total, purified CD4(+) or CD8(+) T cells) failed to improve survival or to induce a granulomato us reaction in infected A beta degrees mice. Survival, cellular and hu moral responses in CD8(+) T-cell-depleted A beta degrees mice or MHC d egrees mice (lacking MHC class I and II molecules) were similar to non depleted A beta degrees mice, suggesting that anti-schistosomula antib ody production was thyme-independent. Our results demonstrate a high d egree of susceptibility of A beta degrees mice to infection and corrob orate the importance of CD4(+) T cells in the initiation of the granul omatous response. However, our results do not show evidence for the in volvement of CD8(+) T cells in response to S. mansoni infection.