Review of the human immune mechanisms directed against Entamoeba histolytica

The human immune mechanisms effective against the destructive parasite Entamoeba histolytica have not been established. Humoral responses develop with invasive disease but have not positively correlated with protection against recurrent invasive infection. Though complement is amebicidal, invasive strains of amebas may be resistant. Polymorphonuclear neutrophils have not been active in vitro against virulent amebic strains and could contribute to the pathogenesis of disease. In vitro studies have shown human activated monocyte-derived macrophages and cytotoxic T lymphocytes to be competent cells in killing virulent amebas. Soluble amebic protein preparations have been shown to be mitogenic for normal, uninfected human lymphocytes, apparently because the N-acetyl-D-galactosamine-inhibitable amebic lectin is present. Despite a lower T4:T8 ratio and a heterogeneous lymphocyte proliferation in response to mitogens, patients with amebic hepatic abscess develop sensitization to amebic antigens and specific effector mechanisms. Although antibody, complement, and nonimmune mechanisms, as well as parasite factors, may be important in determining the occurrence of invasive amebiasis, human cell-mediated immune mechanisms may play a major role in combating invasive infection due to E. histolytica.