Immune deficiency following thermal trauma is associated with apoptotic cell death

J. A. Teodorczyk-Injeyan, M. Cembrzynska-Nowak, S. Lalani, W. J. Peters, G. B. Mills

    Research output: Contribution to journalArticle

    61 Scopus citations


    Thermal injury-associated specific immune deficiency occurs despite indicators of systemic activation of the lymphoid compartment. We investigated the possibility that postburn immune failure and T cell activation are causally related through activation-induced (apoptotic) cell death. The relationship between the cellular immune response and cell mortality was examined in cultures of peripheral blood mononuclear cells (PBMC) from 14 immunosuppressed patients with extensive burns (35-90% total body surface area). Impaired cellular immunity coincided with significantly reduced cell viability as ascertained by propidium iodide staining and dye reduction assays. Following stimulation with the mitogenic lectin, phytohemagglutinin (PHA), the majority of DNA in patient cultures was fragmented, suggesting the occurrence of apoptotic cell death. Even without stimulation a portion of patient cells was apoptotic as indicated by oligonucleosomal bands on agarose gel electrophoresis. Exogenous interleukin-2 or phorbol ester markedly reduced constitutive as well as PHAinduced DNA fragmentation. In situ demonstration of DNA strand breaks in freshly isolated patient PBMC, by a TdT-based labeling technique, confirmed that a larger fraction (up to 60%) of circulating lymphocytes was undergoing apoptosis on the periphery. These novel observations suggest that apoptosis may play a major role in thermal injury-related cellular immunodeficiency.

    Original languageEnglish (US)
    Pages (from-to)318-328
    Number of pages11
    JournalJournal of Clinical Immunology
    Issue number6
    StatePublished - Nov 1 1995


    • Burns
    • T cell activation
    • apoptosis
    • immunodeficiency

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Immunology

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