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

被引:30
作者
Kavanagh, EG [1 ]
Kelly, JL [1 ]
Lyons, A [1 ]
Soberg, CC [1 ]
Mannick, JA [1 ]
Lederer, JA [1 ]
机构
[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Surg Immunol, Boston, MA 02115 USA
关键词
D O I
10.1016/S0039-6060(98)70130-8
中图分类号
R61 [外科手术学];
学科分类号
摘要
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 (IFni-gamma), IL-4, and IL-10 by enzyme-linked immunosorent 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 naive 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 IFN-gamma production by naive CD4+ transgenic T cells, and IL-2 production was marginally reduced. Thus, burn injury primed naive T cells for an enhanced Th1-type response. In contrast, antigen-specific proliferation, IL-2, and IFN-gamma production by T cells ha harvested from immunized wildtype 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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页码:269 / 276
页数:8
相关论文
共 23 条
[1]   Functional diversity of helper T lymphocytes [J].
Abbas, AK ;
Murphy, KM ;
Sher, A .
NATURE, 1996, 383 (6603) :787-793
[2]  
ABLIN RJ, 1981, IMMUNE CONSEQUENCES, P180
[3]   PREDICTING FATAL SEPSIS IN BURN PATIENTS [J].
BAKER, CC ;
MILLER, CL ;
TRUNKEY, DD .
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1979, 19 (09) :641-648
[4]   Surgical stress induces a shift in the type-1/type-2 T-helper cell balance, suggesting down-regulation of cell-mediated and up-regulation of antibody-mediated immunity commensurate to the trauma [J].
Decker, D ;
Schondorf, M ;
Bidlingmaier, F ;
Hirner, A ;
vonRuecker, AA .
SURGERY, 1996, 119 (03) :316-325
[5]  
DING L, 1992, J IMMUNOL, V148, P3133
[6]  
DOBKE M, 1981, IMMUNE CONSEQUENCES, P150
[7]   Hsp60 peptide therapy of NOD mouse diabetes induces a Th2 cytokine burst and downregulates autoimmunity to various beta-cell antigens [J].
Elias, D ;
Meilin, A ;
Ablamunits, V ;
Birk, OS ;
Carmi, P ;
KonenWaisman, S ;
Cohen, IR .
DIABETES, 1997, 46 (05) :758-764
[8]   Interleukin-10 induces a long-term antigen-specific anergic state in human CD4(+) T cells [J].
Groux, H ;
Bigler, M ;
deVries, JE ;
Roncarolo, MG .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (01) :19-29
[9]   BIOLOGICAL PROPERTIES OF INTERLEUKIN-10 [J].
HOWARD, M ;
OGARRA, A .
IMMUNOLOGY TODAY, 1992, 13 (06) :198-200
[10]   Anti-interleukin-10 antibody restores burn-induced defects in T-cell function [J].
Kelly, JL ;
Lyons, A ;
Soberg, CC ;
Mannick, JA ;
Lederer, JA .
SURGERY, 1997, 122 (02) :146-152