Chronic helminth infections induce immunomodulation: consequences and mechanisms.
Worldwide, more than a billion people are infected with helminths. These worm infections generally do not lead to mortality, however, they are chronic in nature and can lead to considerable morbidity. Immunologically these infections are interesting; chronic helminth infections are characterized by skewing towards a T helper 2 type response as well as regulatory responses. The regulatory network is associated with chronic helminth infections and is thought to prevent strong immune responses against parasitic worms, allowing their long-term survival and restricting pathology. This regulatory network is thought to also temper responses to non-helminth antigens, like allergens or self-antigens, possibly leading to lower prevalence of allergies and autoimmune diseases in subjects that are chronically infected with helminths. This raises the interesting idea that helminths may bear molecules that have potential therapeutic action against allergies and possibly other inflammatory diseases. However, on the other side of the coin, this would predict that helminth infected subjects might not respond strongly to third party antigens like vaccines. This is an important issue, since most vaccines that are being developed against diseases such as HIV, tuberculosis or malaria will be introduced in areas where helminth infections are highly prevalent. Moreover, these vaccines are proving difficult to develop and are often weak, thus any confounder that would affect their efficacy needs to be taken into consideration. Helminth derived molecules have been identified that induce T helper 2 and regulatory responses via modulation of dendritic cells and some appear to do so via Toll like receptor (TLR) signaling. New insights into these pathways could be useful to antagonize suppression and hence boost vaccine efficacy or to optimize suppression induced by helminth derived molecules and control inflammatory diseases.
van Riet
Elly
E
Department of Parasitology, Leiden University Medical Centre, Leiden, The Netherlands. p.h.van_riet@lumc.nl
Hartgers
Franca C
FC
Yazdanbakhsh
Maria
M
D000485:Allergens / Q000276:immunology; D000818:Animals; D001324:Autoantigens / Q000276:immunology; D002908:Chronic Disease; D003141:Communicable Diseases / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D006373:Helminthiasis / Q000276:immunology* / Q000401:mortality; D006376:Helminths / Q000276:immunology*; D006790:Host-Parasite Interactions / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D007155:Immunologic Factors / Q000276:immunology*; D015995:Prevalence; D015398:Signal Transduction / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology; D014612:Vaccines / Q000276:immunology / Q000494:pharmacology
D000485:Allergens; D001324:Autoantigens; D007155:Immunologic Factors; D051193:Toll-Like Receptors; D014612:Vaccines