Results obtained from studies using interleukin (IL)-10 antagonism to block the action of endogenous IL-10 in animal models of systemic and local infection or inflammation induced by lipopolysaccharide (LPS) administration have provided convincing evidence which links the role played by IL-10 in modulating fever and sickness behavior to it suppressing the synthesis of key mediators known to induce sickness responses, namely pro-inflammatory cytokines[1-3]. Here, IL10 is linked to infection.