Bladder for environmental release. Similarly, filarial vive remalas poorly understood despite eos...
bladder for environmental release. Similarly, filarial vive remalas poorly understood despite eosinophils having infective larvae and parasitization by long-lived adul worms capable of continuously releasing microfilariae that circulate in the bloodstream or migrate through sub- Although it has long been beld that the primary function of the cosiaophil is prodection against helminth parasites, there are little data to prove this anequivocally. Moreover Because each stage of parasite development can be nflammatory pathology accompany ing helminth infectios parasite provide an overvicw of oar currenst knom lantigenically distinct, the host response to helminth infection is often characterized by a series of discrete about eesinophils and their role, both protective and patho immune responses that evolve at different times during the course of infection. Protective immunity directed against a single stage might be circumvented by parasite differentiation, assisting in the survival of the pathogen Immanol 2004 113:30-7) age of parasite development might also entail a change in tissue trophism, introducing a or multicellular helminths (worms), the extraordinary worldwide prevalence of which exacts a major medical resistance. Each st compartmental feature to immune or inflammat example, a variety of distinct cutaneous, micrometers in size, whereas helminths are typically cen- pulmonary, and intestinal inflammatory or hyper- ling protozoa are eosinophilic syndromes are associated with different often intracellular parasites at some stage of infection, stages of Ascaris and Strongy loides species as they whereas helminths, being larger than most tissue cells, are migrate through the skin and lung before reaching adult diverse and unique biology. Protozoa are usually a few responses. For almost always extracellular pathogens, with the signifi- hood in t Because complex parasitic life cycles can only be main- tained by sequential passage through intermediate and cant exception being Trichinella spiralis. Although proto- B zoa usually replicate during infection of a single host, helminths do not reproduce without the passage through definitive hosts, parasites have adapted methods of opti mizing transmission by prolonging infection. Perhaps because of this evolutionary pressure, chronicity, latency le infection, the or both are hallmarks of helminth infections. For example to larval-, adult-, or adult schistosomes and filariae can survive in host tissues free-swimming cercari- for as long as 20 to 30 years, continuously producing eges trate the and larvac. Strongy loides species, because of their ability ts immersed in infested water and to "autoinfect," maintain their life cycle for decades. infection. In the course of a singl of the trematode Schistosoma mansoni penetrate liver and mesenteric veins for further differentiation into sitism" in that inducing mortality in the host would disrupt the host were to die before egg lay sexually dimorphic adult worms. Eggs are laid that parasite transmission if migrate through tissues into the lumen of the bowel or ing or larval release could occur. Adaptations for chronic- ity can be so successful among parasites that naturally acquired protective immunity is only observed rarely in areas endemic for a given disease. Specifically, schistoso- miasis results in an incomplete form of protection in which nstithute of Allagy and Infectious Diseases, National Institutes of reinfection is limited but adult worms are tolerated for Recenved for pubication October 20, 2003, revised Oetober 20,2003, accept Whereas pathology and protective immunity to most From the Helminth Immunology Section, Laboratory of Parasitic Diseases protozoa are believed to reflect T cell-, B cell-, and Reprint requests Thomas B. Nutman, MD, Laboratory of Parasitic Discase macrophage-dependent (or perhaps cytokine-mediated) mechanisms, infection with helminth parasites induces Building 4, Room B1-03, 4 Center Dr, National Institules of Health doi 10.1016j jaci 2003 10 050 immune effector responses that are characterized by lgE
bladder for environmental release. Similarly, filarial vive remalas poorly understood despite eosinophils having infective larvae and parasitization by long-lived adul worms capable of continuously releasing microfilariae that circulate in the bloodstream or migrate through sub- Although it has long been beld that the primary function of the cosiaophil is prodection against helminth parasites, there are little data to prove this anequivocally. Moreover Because each stage of parasite development can be nflammatory pathology accompany ing helminth infectios parasite provide an overvicw of oar currenst knom lantigenically distinct, the host response to helminth infection is often characterized by a series of discrete about eesinophils and their role, both protective and patho immune responses that evolve at different times during the course of infection. Protective immunity directed against a single stage might be circumvented by parasite differentiation, assisting in the survival of the pathogen Immanol 2004 113:30-7) age of parasite development might also entail a change in tissue trophism, introducing a or multicellular helminths (worms), the extraordinary worldwide prevalence of which exacts a major medical resistance. Each st compartmental feature to immune or inflammat example, a variety of distinct cutaneous, micrometers in size, whereas helminths are typically cen- pulmonary, and intestinal inflammatory or hyper- ling protozoa are eosinophilic syndromes are associated with different often intracellular parasites at some stage of infection, stages of Ascaris and Strongy loides species as they whereas helminths, being larger than most tissue cells, are migrate through the skin and lung before reaching adult diverse and unique biology. Protozoa are usually a few responses. For almost always extracellular pathogens, with the signifi- hood in t Because complex parasitic life cycles can only be main- tained by sequential passage through intermediate and cant exception being Trichinella spiralis. Although proto- B zoa usually replicate during infection of a single host, helminths do not reproduce without the passage through definitive hosts, parasites have adapted methods of opti mizing transmission by prolonging infection. Perhaps because of this evolutionary pressure, chronicity, latency le infection, the or both are hallmarks of helminth infections. For example to larval-, adult-, or adult schistosomes and filariae can survive in host tissues free-swimming cercari- for as long as 20 to 30 years, continuously producing eges trate the and larvac. Strongy loides species, because of their ability ts immersed in infested water and to "autoinfect," maintain their life cycle for decades. infection. In the course of a singl of the trematode Schistosoma mansoni penetrate liver and mesenteric veins for further differentiation into sitism" in that inducing mortality in the host would disrupt the host were to die before egg lay sexually dimorphic adult worms. Eggs are laid that parasite transmission if migrate through tissues into the lumen of the bowel or ing or larval release could occur. Adaptations for chronic- ity can be so successful among parasites that naturally acquired protective immunity is only observed rarely in areas endemic for a given disease. Specifically, schistoso- miasis results in an incomplete form of protection in which nstithute of Allagy and Infectious Diseases, National Institutes of reinfection is limited but adult worms are tolerated for Recenved for pubication October 20, 2003, revised Oetober 20,2003, accept Whereas pathology and protective immunity to most From the Helminth Immunology Section, Laboratory of Parasitic Diseases protozoa are believed to reflect T cell-, B cell-, and Reprint requests Thomas B. Nutman, MD, Laboratory of Parasitic Discase macrophage-dependent (or perhaps cytokine-mediated) mechanisms, infection with helminth parasites induces Building 4, Room B1-03, 4 Center Dr, National Institules of Health doi 10.1016j jaci 2003 10 050 immune effector responses that are characterized by lgE