The finding that partially matured DCs respond to TLR2 stimulation with an anti-inflammatory program could shed light on why patients with severe sepsis undergo long-term systemic and local immunosuppression despite their increased TLR2 expression (Armstrong et al., 2004), and how TLR2-derived signals from Candida albicans or Schistosome infections drive immunosuppression by IL-10 production and Treg induction (van der Kleij et al., 2002; Netea et al., 2004). The gene discussed is TLR2; the disease is Sepsis.