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Kelly John L.; O'Suilleabhain, Criostoir B.; Soberg, Christopher C.; Mannick, John A.; Lederer, James A.
Shock: July 1999
Original Article: PDF Only


Although it is established that post-injury immune dysfunction involves alterations in T-cell function, the effects of injury on T-cell function in vivo are poorly understood. This study uses a mouse injury model and an antigen immunization approach to investigate the influence of injury on antigen-specific T-helper cell function. We report here that injury triggered a significant reduction in antigen-specific T-helper-1 (Th1)-dependent lgG2a antibody formation, while IgM, lgG1, and IgE production was unchanged. In addition, injury caused a reduction in cytokine production (IL-2, IFN± and IL-10) by antigen-stimulated T-cells. We also demonstrate that interleukin 12 (IL-12), a cytokine that promotes Th1 cell differentiation, restored lgG2a antibody formation and corrected the injury-induced reduction in antigen-stimulated cytokine production. Taken together, these findings indicate that severe injury induces a dramatic reduction in Th1 cell function in vivo and suggest that therapies designed to restore Th1 cell function may be beneficial to the injured host.

©1999The Shock Society