Helminth infections appear to play an important role in modulating the immune response in TB.1 Co-infection with helminths may contribute to the poor outcome of M. tuberculosis infection by skewing the immune response to the production of immunoglobulin (Ig) E antibodies, which is IL-4 dependent.7 Adjobimey et al. showed that high plasma concentrations of IgG4 in patients with filaria were associated with hypo-responsiveness, high parasite load and high plasma levels of IL-10 and TGF-β.8 This evidence concerns the gene TGFB1 and tuberculosis.