Helminth Infections Prevent Autoimmune Diseases through Th2-Type Immune Response

Helminth parasites are known to elicit the immune response towards T helper 2 (Th2)-type, characterized by Th2 related cytokines, that typically include interleukin-4 (IL-4), IL-5 and IL-13. In this review we will describe the mechanisms involved in helminth induced Th2 immune response. Intestinal epithelial cells (IECs) produce thymic stromal lymphopoietin (TSLP), which is both necessary and sufficient for the initiation of Th2 cytokine-driven inflammation. IL-33 mRNA is expressed early during parasite infection and IL-33 binds ST2 receptor, both of which are associated with optimal CD4+ Th2 polarization. Following innate immune cell recognition, basophils and mast cell can secrete Th2 type cytokines that are thought to contribute to CD4+ Th2 differentiation. Additionaly, dendritic cell conditioned with some helminth products can promote CD4+ Th2 differentiation. Alternatively activated macrophages, activated by the Th2 cytokines IL-4 and IL-13 in parasitic infections, contribute to the host protective response: control of Th1-type inflammation, wound healing and worm expulsion. Experimentally, helminths have been associated with protection against a number of autoimmune disorders, including inflammatory bowel diseases and type 1 diabetes. It may be a novel strategy to ameliorate autoimmune inflammation by expanding and activating the Th2 response originated from parasites

Natural infection of Plasmodium falciparum induces inhibitory antibodies against gametocyte development in human hosts.

SUMMARY: We identified naturally induced antibodies from malaria patients in Thailand and clarified the effect of the antibodies on gametocyte development. Fifty-nine percent of the Plasmodium falciparum-infected blood samples (17 of 29) fed to female Anopheles mosquitoes showed no oocyst infection. Seventeen percent of the samples (5 of 29) distorted the morphology and hampered the maturity of the gametocytes. A possible mechanism for the gametocyte inhibitory activity was shown by the binding of the plasma antibodies to live, immature, intraerythrocytic gametocytes during the incubation period. One hundred fifty-seven proteins specific to different gametocyte stages were explored to find the targets of the antisera that bound to the live gametocytes. However, no additional gametocyte transmission-blocking vaccine candidate was detected. Therefore, the development of alternative transmission-blocking vaccines in high-transmission areas should focus on the identification of more gametocyte antigens-inducing inhibitory antibodies that reduce gametocytemia

Observation of morphological changes of female osmiophilic bodies prior to Plasmodium gametocyte egress from erythrocytes

Plasmodium parasites cause malaria in mammalian hosts and are transmitted by Anopheles mosquitoes. Gametocytes, which differentiate from asexual-stage parasites, are activated by environmental changes when ingested into the mosquito midgut, and are rapidly released from erythrocytes prior to fertilization. Secretory proteins localized to osmiophilic bodies (OBs), organelles unique to gametocytes, have been reported to be involved in female gametocyte egress. In this study, we investigate the dynamics of OBs in activated gametocytes of Plasmodium falciparum and Plasmodium yoelii using the female OB-specific marker protein, G377. After activation, female gametocyte OBs migrate to the parasite surface and fuse to form large vesicles beneath the parasite plasma membrane. At the marginal region of female gametocytes, fused vesicles secrete contents by exocytosis into the parasitophorous vacuole space, prior to parasite egress via the break-down of the erythrocyte membrane. This is the first detailed description of how proteins are transported through osmiophilic bodies