Interleukin 10 is not essential for survival or for modulating T-cell function after injury

Background. Interleukin 10 (Il-10) is thought to be protective injury and s epsis. However, we recently reported that Il-10 antagonism can be beneficia l after burn injury. This study used IL-10-deficient (IL-10 [-/-]) mice to further define the role of IL-10 after injury. Methods. Wild-type (WT) C57BL/6 or Il-10 (-/-) mice were anesthetized, sham or burn injured, and immunized subcutaneously with a T-cell-dependent prot ein antigen. Ten days later antigen-specific serum antibody isotype formati on was measured by enzyme-linked immunosorbent assay. In addition, antigen- stimulated splenic T-cell proliferation and cytokine production (interleuki n 2, interferon gamma, and tumor necrosis factor-alpha) were measured. Results. Burn-injured IL-10 (-/-) mice survival (80%) was equivalent to tha t of burn-injured WT mice (74%). An injury-dependent loss of T-helper 1 (Th 1)-type antibody isotype (IgG2a) formation occurred in both WT and IL-10 (- /-) mice. In vitro studies indicated that burn injury caused reduced antige n-stimulated splenic T-cell proliferation and Th 1-type (interleukin 2 and interferon gamma) cytokine production in WT and IL-10 (-/-) mice, whereas b urn-injured Il-10 (-/-) mice produced high levels of antigen-stimulated tum or necrosis factor-alpha. Conclusions. Il-10 is not essential for survival after burn injury or for s everal injury-induced changes in adaptive immune function, including Th1-ty pe antibody isotype formation, T-cell proliferation, and Th1-type cytokine production.