Netea et al. (2004) reported that the absence of the TLR2 receptor had a beneficial role during Candida albicans infection, leading to resistance to disseminated candidiasis, with normal production of pro-inflammatory cytokines, such as TNF-α, IL-1α, and IL-1β, by peripheral adherent cells, and a decrease in the levels of IL-10 and CD4+CD25+ T lymphocytes. The gene discussed is IL1B; the disease is disseminated candidiasis.