Citation

Kelly JL, O'Suilleabhain CB, Soberg CC, Mannick JA, Lederer JA. Shock 1999; 12(1): 39-45.

Affiliation

Department of Surgery (Immunology), Harvard Medical School/Brigham and Women's Hospital, Boston, MA 02115, USA.

Copyright

(Copyright © 1999, The Shock Society, Publisher Lippincott Williams and Wilkins)

DOI

unavailable

PMID

10468050

Abstract

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 IgG2a antibody formation, while IgM, IgG1, and IgE production was unchanged. In addition, injury caused a reduction in cytokine production (IL-2, IFNgamma and IL-10) by antigen-stimulated T-cells. We also demonstrate that interleukin 12 (IL-12), a cytokine that promotes Th1 cell differentiation, restored IgG2a 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.

Language: en