title: Interleukin 10 is not essential for survival or for modulating T-cell function after injury.
abstract: BACKGROUND
  Interleukin 10 (IL-10) is thought to be protective in injury and sepsis. However, we recently reported that IL-10 antagonism can be beneficial 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 protein antigen. Ten days later antigen-specific serum antibody isotype formation was measured by enzyme-linked immunosorbent assay. In addition, antigen-stimulated splenic T-cell proliferation and cytokine production (interleukin 2, interferon gamma, and tumor necrosis factor-alpha) were measured.
  
  
  RESULTS
  Burn-injured IL-10 (-/-) mice survival (80%) was equivalent to that of burn-injured WT mice (74%). An injury-dependent loss of T-helper 1 (Th1)-type antibody isotype (IgG2a) formation occurred in both WT and IL-10 (-/-) mice. In vitro studies indicated that burn injury caused reduced antigen-stimulated splenic T-cell proliferation and Th1-type (interleukin 2 and interferon gamma) cytokine production in WT and IL-10 (-/-) mice, whereas burn-injured IL-10 (-/-) mice produced high levels of antigen-stimulated tumor necrosis factor-alpha.
  
  
  CONCLUSIONS
  IL-10 is not essential for survival after burn injury or for several injury-induced changes in adaptive immune function, including Th1-type antibody isotype formation, T-cell proliferation, and Th1-type cytokine production.
authors.affiliation: Department of Surgery, Harvard Medical School, Brigham and Women's Hospital, Boston, Mass. 02115, USA.
authors.forename: E K
authors.initials: EK
authors.lastname: Kavanagh
authors.forename: M R
authors.initials: MR
authors.lastname: Kell
authors.forename: A
authors.initials: A
authors.lastname: Goebel
authors.forename: C C
authors.initials: CC
authors.lastname: Soberg
authors.forename: J A
authors.initials: JA
authors.lastname: Mannick
authors.forename: J A
authors.initials: JA
authors.lastname: Lederer
mesh_terms: D000818:Animals; D000917:Antibody Formation; D002056:Burns / Q000276:immunology / Q000401:mortality*; D016207:Cytokines / Q000096:biosynthesis; D007108:Immune Tolerance; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D013601:T-Lymphocytes / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma