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 . 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 ), 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.