Abstract
The depression in cell-mediated immunity following severe injury contributes to increased sepsis and mortality. The possible mechanisms behind the development of immune dysfunction include the generation of suppressor T-cell subpopulations [1], decreased helper T-cell function [2], the appearance of immunosuppressive factors [3], depressed interleukin-2 production and receptor expression [2, 4], and enhanced activation of prostaglandin pathways [4, 5]. The maintenance of normal T-cell activities and proliferation is obviously disrupted prior to and following these changes in the immune system. Recent studies have shown that after thermal injury T-cell clonal expansion is depressed because of reduced production of and response to interleukin-2 [6].
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References
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© 1989 Springer-Verlag, Berlin Heidelberg
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Gadd, M.A., Soderberg, C.S., Ozkan, A.N., Hansbrough, J.F. (1989). Lymphocyte Surface Antigen Expression Following Lectin Stimulation: An Index of Early T-Cell Dysfunction After Controlled Murine Injury. In: Faist, E., Ninnemann, J.L., Green, D.R. (eds) Immune Consequences of Trauma, Shock, and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73468-7_15
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DOI: https://doi.org/10.1007/978-3-642-73468-7_15
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