| Summary: | Helminths are credited with being the major selective force driving the evolution of the so called type 2 immune responses in vertebrate animals, with their size and infection strategies presenting unique challenges to the immune system. Originally, type 2 immune responses were defined by the presence and activities of the CD4+ T helper 2 subset producing the canonical cytokines IL-4, IL-5 and IL-13. This picture is now being challenged by the discovery of a more complex pattern of CD4+ T helper cell subsets that appear during infection, including Tregs, Th17, Tfh and more recently Th22, Th9, and ThGM. In addition, a clearer view of the mechanisms by which helminths and their products selectively prime the CD4+ T cell subsets is emerging. In this review, we have focused on recent new data concerning the selective priming, differentiation and functional role of CD4+ T helper cell subsets in the context of helminth infection. We argue for a re-evaluation of the original Th2 paradigm and discuss how the observed plasticity of the T helper subsets may enable the parasitized host to achieve an appropriate compromise between elimination, tissue repair, containment and pathology.
|
|---|
