Parasite immunity: Pathways for expelling intestinal helminths

The immune system is dependent upon a web of small soluble protein molecules that modulate a wide range of potent immune effector mechanisms. These mediators, or cytokines, are secreted by distinct subsets of cells, and exert differential effects on the immune system [1]. Two such groups of cytokines are derived from T cells: type 1 cytokines are broadly inflammatory, and include interferonγ (IFN-γ) and tumour necrosis factor-β (TNF-β); type 2 cytokines, such as interleukin-4 (IL-4), IL-5, IL-6, IL-10 and IL-13, promote B-cell and granulocyte growth and differentiation. This designation parallels the typical helper T-cell subsets from which these cytokines are produced: Th1 cells secrete IFN-γ and TNF-β, whereas Th2 secrete the type 2 cytokines. Cytokines produced by Th1 and Th2 cells have opposing effects: the type 1 cytokine IFN-γ directly downregulates Th2 cells, while the type 2 cytokine IL-4 indirectly blocks Th1 cell expansion. A Th1 response can thus be artificially favoured by providing either exogenous IFN-γ or anti-IL-4 neutralising antibodies.