Human Schistosome Infection and Allergic Sensitisation

Figure 1

Possible regulatory mechanisms in helminth infections. Primary response (a) to parasite antigens involves Th2 polarization, IgE production, and eosinophil, mast cell, and basophil activation (I), mechanisms similar to those observed in allergic sensitisation (c). This Th2-response may be induced by parasite-secreted antigens such as the Omega-1 secreted by S. mansoni eggs [25]. However, with increasing parasite load or chronic infection (b), regulatory B cells are activated which suppress Th2 responses (II) via IL-10 secretion or CD23 expression [26], and/or contribute to the recruitment of Tregs [27]. Tregs (III), which may also be induced and expanded by parasite antigens [28, 29], either induce anergic Th2 cells (expressing GITR and CTLA4) unable to progress through to effector cells, or modify downstream effector functions such as B cell switch to IgG4 and/or alternative activation of macrophages, resulting in immunological tolerance (reviewed by [30]). This immunosuppression is induced in the context of helminth infection, but may also expand to allergen-induced inflammation (gray line), hence suppressing allergy. DC: dendritic cell; B: B cell, Eos: eosinophil; Bas: basophil; MC: mast cell; GITR: glucocorticoid-induced TNFα-related protein; CTLA4: cytotoxic T lymphocyte antigen 4; AAM: alternatively activated macrophage; Breg: regulatory B cell; Treg: regulatory T cell. The question mark (?) denotes lack of strong evidence. Figure adapted from [30, 31] and collated information from the cited references.