Factors that modify the cellular-immune response in patients infected by <i>Schistosoma mansoni</i>.

Abstract

Abstract Cell-mediated immunity (CMI) to soluble egg antigen (SEA) and tuberculin purified protein derivative (PPD) was evaluated by means of in vitro lymphocyte proliferation and quantitation of in vivo granuloma size in 31 Kenyan children (ages 7 to 16) with Schistosoma mansoni infection. Although antigen-induced proliferative responses varied from patient to patient, a statistically significant (p &amp;lt; 0.05) direct correlation was observed between the granuloma size and the degree of proliferation. In contrast, the SEA-induced proliferative response varied inversely with the titer of anti-MSA1 antibodies. Possible humoral and cellular factors that could explain the heterogeneity in CMI responses observed in the first study were investigated in a subsequent study involving 34 children. It was found that lymphocytes from some patients cultured in the presence of autologous serum proliferated significantly less to SEA than in the presence of normal AB positive serum. However, proliferative responses to tuberculin PPD were less inhibited by autologous serum. Of particular interest, SEA-anti-SEA complexes were detected in the sera of 7 patients. Proliferation to SEA (but not PPD) and the size of granulomas were significantly lower in these latter patients compared with those without antigen-antibody complexes. The presence of antigen-specific suppressor cells was investigated using a co-culture technique. Suppressor cells were activated in vitro by preculture with SEA or PPD. Mononuclear cells from 19 patients preincubated with SEA significantly suppressed the proliferative response to SEA much more than to PPD (61% vs 27% inhibition). The use of PPD to activate suppressor cells resulted in nonspecific inhibition, suppressing the PPD proliferative response to the same extent as the SEA response. Proliferation in response to SEA in the absence of co-culture was statistically lower and anti-MSA1 titers were higher in patients with SEA suppressors than in patients without evidence of SEA-specific suppressor cells. These results imply that there are several factors that affect the CMI response to SEA in patients during the course of infection, including factors present in serum (possibly antigen-antibody complexes) and the presence of antigen-specific suppressor cells.