Literature DB >> 9706148

Burn injury primes naive CD4+ T cells for an augmented T-helper 1 response.

E G Kavanagh1, J L Kelly, A Lyons, C C Soberg, J A Mannick, J A Lederer.   

Abstract

BACKGROUND: The mechanisms responsible for altered T-cell responses and cytokine production after injury are not well understood. We used T-cell receptor (TCR) transgenic mice to study burn injury effects on naive versus antigen-activated CD4+ T cells in vivo.
METHODS: One week after sham or burn injury, lymph node cells were prepared from TCR transgenic mice and stimulated with TCR transgene-specific antigens. T-cell proliferation was measured and culture supernatants were tested for interleukin-2 (IL-2), interferon-gamma (IFN-gamma), IL-4, and IL-10 by enzyme-linked immunosorbent assay (ELISA). Burn injury effects on antigen-activated T cells were studied by immunizing TCR transgenic or wild-type mice at the time of injury.
RESULTS: The antigen-stimulated proliferation of native CD4+ T cells was unaffected by burn injury and no increase in T-helper 2 (Th2)-type cytokine production was observed. Instead, burn injury augmented INF-gamma production by naive CD4+ transgenic T cells, and IL-2 production was marginally reduced. Thus, burn injury primed native T cells for an enhanced Th1-type response. In contrast, antigen-specific proliferation, IL-2, and IFN-gamma production by T cells harvested from immunized wild-type mice were suppressed. Unexpectedly, high mortality was observed when burn-injured TCR transgenic mice were immunized.
CONCLUSION: Our results show that burn injury has differential effects on naive and antigen-activated CD4+ T cells and can prime naive CD4+ T cells.

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Year:  1998        PMID: 9706148

Source DB:  PubMed          Journal:  Surgery        ISSN: 0039-6060            Impact factor:   3.982


  8 in total

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8.  Increased oxidative phosphorylation in lymphocytes does not atone for decreased cell numbers after burn injury.

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  8 in total

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