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Long-term infection with parasitic worms is generally associated with an immunological phenotype that is Th2-like and anti-inflammatory. This phenotype is probably an unintentional consequence of molecular characteristics of worms (as free-living worms also express polarising molecules) in combination with deliberate attempts by the parasites, via molecular secretions, to modulate the phenotype. This review is concerned with the identity of immunomodulatory worm products, the receptors that they interact with and the signal transduction pathways that they activate. It hopes to indicate how knowledge of these factors can explain the changes in gene expression that result in the characteristic worm-induced immunological phenotype.
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Harnett et al. (2006) studied this question.
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