Consistent with this, dermal conditioning of antigen-presenting cells by eosinophils during multiple larval infections of the skin further down-regulates the TH1 response in a mechanism requiring a recruitment of large numbers of RELM-α + eosinophils providing an enriched TH2 cytokine (IL-4, IL-13) skin microenvironment that conditions DC and macrophage populations that can subsequently impact negatively on egg granuloma size in the liver [93]. The gene discussed is IL4; the disease is infection.