THE ROLE OF CD4(-CELLS IN HOST MORBIDITY AND INNATE RESISTANCE TO ANGIOSTRONGYLUS-CANTONENSIS IN THE MOUSE() AND CD8(+) T)

Strain-dependent differences in host morbidity and mortality due to An giostrongylus cantonensis infection have been established between C57B L/6 and BALB/c mice; C57BL/6 mice show rapid worm killing with low mor bidity, whereas BALB/c mice indicate slow worm killing with high morbi dity and mortality. To determine the possible roles of CD4(+) and CD8( +) T-cells in host morbidity and innate resistance to A. cantonensis i nfection we treated C57BL/6 and BALB/c mice with anti-CD4 or anti-CD8 monoclonal antibody and examined the changes in host morbidity and wor m-killing activity. Our study indicates that anti-CD4 antibody treatme nt interferes with worm killing and improves the morbidity of A. canto nensis-infected BALB/c mice, whereas anti-CD8 antibody treatment fails to improve the morbidity. Tumor necrosis factor-alpha (TNF-alpha, or cachectin) production in infected mice was not correlated with host mo rbidity. Anti-IL-5 monoclonal antibody treatment also failed to affect the morbidity of infected BALB/c mice, although their worm-killing ac tivity was restrained as shown in anti-CD4-treated mice. These finding s clearly indicate that the morbidity of infected BALB/c mice is regul ated by some unknown CD4(+) T-cell-dependent mechanism but not by an I L-5-, eosinophil-, or TNF-alpha-dependent mechanism.