Literature DB >> 1403109

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors.

K B Quattrocchi1, C H Miller, F C Wagner, S J DeNardo, G L DeNardo, K Ovodov, E H Frank.   

Abstract

Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factor(s) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

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Year:  1992        PMID: 1403109     DOI: 10.3171/jns.1992.77.5.0694

Source DB:  PubMed          Journal:  J Neurosurg        ISSN: 0022-3085            Impact factor:   5.115


  10 in total

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2.  Surgical denervation of ocular sympathetic afferents decreases local transforming growth factor-beta and abolishes immune privilege.

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5.  Safety and tolerability of cyclosporin a in severe traumatic brain injury patients: results from a prospective randomized trial.

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6.  Early or Late Bacterial Lung Infection Increases Mortality After Traumatic Brain Injury in Male Mice and Chronically Impairs Monocyte Innate Immune Function.

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Review 7.  The duality of the inflammatory response to traumatic brain injury.

Authors:  P M Lenzlinger; M C Morganti-Kossmann; H L Laurer; T K McIntosh
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Review 8.  Inflammatory response following diffuse axonal injury.

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Journal:  Int J Med Sci       Date:  2013-03-13       Impact factor: 3.738

Review 9.  Nosocomial infections and immunity: lesson from brain-injured patients.

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Review 10.  Traumatic Brain Injury and Peripheral Immune Suppression: Primer and Prospectus.

Authors:  Jon Hazeldine; Janet M Lord; Antonio Belli
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  10 in total

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