Secretory products of helminth parasites as immunomodulators.
Parasitic helminths release molecules into their environment, which are generally referred to as excretory-secretory products or ES. ES derived from a wide range of nematodes, trematodes and cestodes have been studied during the past 30-40 years, their characterization evolving from simple biochemical procedures such as SDS-PAGE in the early days to sophisticated proteomics in the 21st century. Study has incorporated investigation of ES structure, potential as vaccines, immunodiagnostic utility, functional activities and immunomodulatory properties. Immunomodulation by ES is increasingly the area of most intensive research with a number of defined helminth products extensively analyzed with respect to the nature of their selective effects on cells of the immune system as well as the molecular mechanisms, which underlie these immunomodulatory effects. As a consequence, we are now beginning to learn the identities of the receptors that ES employ and are increasingly acquiring detailed knowledge of the signalling pathways that they interact with and subvert. Such information is contributing to the growing idea that the anti-inflammatory properties of a number of ES products makes them suitable starting points for the development of novel drugs for treating human inflammatory disease.
Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, United Kingdom. Electronic address: w.harnett@strath.ac.uk.
William
W
Harnett
D000818:Animals; D015801:Helminth Proteins / Q000235:genetics / Q000276:immunology*; D006373:Helminthiasis / Q000276:immunology* / Q000469:parasitology; D006376:Helminths / Q000235:genetics / Q000276:immunology*; D006790:Host-Parasite Interactions; D006801:Humans; D010271:Parasites / Q000235:genetics / Q000276:immunology*; D021381:Protein Transport; D055571:Secretory Pathway
D015801:Helminth Proteins
Cell signalling; Excretory-secretory product; Immunomodulation; Parasitic helminth; Regulatory immune response; Th2 response