Unique Identifier : AIDSLINE MED/99396126
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.
JOURNAL ARTICLE Animal Antibody Formation Antigen Presentation
Burns/*IMMUNOLOGY *Immunity