Figure 5

A map of T cell-mediated responses to pathogens. Three effector subsets, Th1, Th2, Th17, and the regulatory Treg are characterized by distinct cytokine profiles [73]. All three pro-inflammatory subsets reciprocally antagonize each other as indicated with a grey triangle in the centre where they were shown to overlap. Treg cells, represented with a black three-pointed star superimposed at the centre of the figure, inhibit all three Th subsets, thus preventing excessive inflammatory responses. T cell-mediated responses represent combined immune responses, which include both innate and adaptive components. Immune response to most bacterial and viral pathogens is generally pro-inflammatory. The Th1 cells secrete interferon γ (IFNγ) and IL-12, which protect against viral infections and other intracellular pathogens. Th17 is a highly pro-inflammatory arm characterised by rapid induction of neutrophils at the inflamed tissue and requires IL-1 and IL-6 for its activation. In contrast, parasitic infections drive Th2 immune responses characterized by production of IL-4 and IL-13, which mediate elimination of multicellular parasites. In addition to driving polarized Th2 responses, parasitic infections are associated with the induction of Tregs and immunoregulatory IL-10, which can induce immune anergy. The resultant effect of this is that parasitic infections can be characterized by an overall down-regulated immune system and therefore modified Th2-response, termed Th2-like. Because many cytokines can be produced and utilised by a number of different cells (IL-10 being a good example [106]), it is clear that multiple cell types may contribute to the regulation of the type and extent of inflammation. Thus, immune regulation likely depends on the specific combination of different T cells called upon during an infection than on a clear predominance of one response profile.