It has been shown that active tuberculosis (TB) drives BTLA expression in DCs, leading to reduced expression of DC-maturation markers, decreased IL-12/IFNα production, and increased IL-4 and TGFβ production, and in consequence to suppression of Th17 and Th22 response while promoting Th2 and Foxp3 + Treg differentiation [46]. The gene discussed is IL4; the disease is tuberculosis.