Immunity to Parasites

Parasites such as protozoa or helminths currently account for greater morbidity and mortality than any other class of infectious organisms, particularly in developing countries. The structural and antigenic diversity of pathogenic parasites is reflected in the heterogeneity of the adaptive immune responses that they elicit. Protozoa that live within host cells are destroyed by cell-mediated immunity, whereas helminths are eliminated by IgE antibody and eosinophil mediated killing as well as by other leukocytes. The principal innate immune response to protozoa is phagocytosis, but many of these parasites are resistant to phagocytic killing and may even replicate within macrophages. Phagocytes also attack helminthic parasites and secrete microbicidal substances to kill organisms that are too large to be phagocytosed. Some helminths may also activate the alternative pathway of complement. The principal defense mechanism against protozoa that survive within macrophages (e.g. Leishmania spp., Toxoplasma gondii) is cell-mediated immunity, particularly macrophage activation by TH1 cell-derived cytokines. Protozoa that replicate inside various host cells and lyse these cells stimulate specific antibody and cytotoxic T lymphocytes (CTL) responses (e.g. Plasmodium spp.). Defense against many helminthic infections is mediated by the activation of TH2 cells, which results in production of IgE antibodies and activation of eosinophils and mast cells. The combined actions of mast cells and eosinophils lead to expulsion and destruction of the parasites. Most parasitic infections are chronic because of weak innate immunity and the ability of parasites to evade or resist elimination by adaptive immune responses Parasites evade the immune system by varying their antigens during residence in vertebrate hosts, by acquiring resistance to immune effector mechanisms, and by masking and shedding their surface antigens.