Neutralization of endogenously produced IL-10 by administration of anti-IL-10 monoclonal antibody 2 h before LPS challenge resulted in a marked increase in both TNF-α and IFN-γ serum levels, and high mortality rates [19], suggesting that the rapid release of IL-10 during endotoxemia is a natural antiinflammatory response controlling cytokine production and LPS toxicity. The gene discussed is IL10; the disease is serum lipopolysaccharide activity.