Immunological Response of Major Histocompatibility Complex Class II‐Deficient (Aβ°) Mice Infected by the Parasite Schistosoma mansoni

We have characterized the immunological behaviour of major histocompitibility complex (MHC) Class II molecule‐deficient (Aβ°) mice after infection by Schistosoma mansoni. In Aβ° mice, morbidity developed dramatically 7 weeks after infection leading to death, despite the absence of an increase in parasite burden or of eggs trapped in the liver. Histological examination of the liver revealed the absence of a classical granulomatous reaction. Antibodies were produced only against schistosomulum antigens. Specific antibodies against adult worm (SWAP) or egg antigen (SEA) were not detected. Cytokine production (IFN‐γ and IL‐4) was absent after in vitro restimulation of splenic cells from infected Aβ° 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 granulomatous reaction in infected Aβ° mice. Survival, cellular and humoral responses in CD8+ T‐cell‐depleted Aβ° mice or MHC° mice (lacking MHC class I and II molecules) were similar to nondepleted Aβ° mice, suggesting that anti‐schistosomula antibody production was thymo‐independent. Our results demonstrate a high degree of susceptibility of Aβ° mice to infection and corroborate the importance of CD4+ T cells in the initiation of the granulomatous response. However, our results do not show evidence for the involvement of CD8+ T cells in response to S. mansoni infection.