Immune Dysfunction in Silicosis: A Hypothesis
Public Domain
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1996/07/01
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Description:This review described the hypothesis that cytokine networking between macrophages and lymphocytes induces the dysregulation of helper T-cell interactions in the lung disease silicosis, resulting in the enhancement of antibody responses and the suppression of cell mediated immunity. The clinical manifestations of silicosis, and the potential roles of helper T-cells and macrophages in silicosis associated immune dysfunction were described. Dysregulated and increased immunoglobulin production, as well as impaired host defense against mycobacteria are important features of silicosis associated immune dysfunction. Because normal host defense against mycobacteria occurs via the cell mediated delayed type hypersensitivity responses of T-lymphocytes and macrophages, it is probable that silicosis is associated with the in-vivo functional impairment of T-lymphocytes or macrophages, or both. The stimulation of antibody production and the downregulation of delayed hypersensitivity responses results from the underlying mechanism of regulation and crossregulation via the CD4+ T-cell subsets TH1 and TH2. The role of macrophages in affecting immune performance relates to their production of immunomodulatory products such as tumor necrosis factor-alpha, interleukin-1, and interleukin-6. Counterregulation by Immunoglobulin-4 was also discussed in the theory that macrophages participate in the genesis of immune dysfunction in silicosis, both by the secretion of directly immunomodulating cell products and by cytokine networking with helper T-cells. The authors conclude that silica (14808607) is pathogenic in both the induction of pulmonary fibrosis and the induction of immune dysfunction. [Description provided by NIOSH]
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ISSN:1047-322X
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Volume:11
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Issue:7
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NIOSHTIC Number:nn:00235412
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Citation:Appl Occup Environ Hyg 1996 Jul; 11(7):962-965
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Federal Fiscal Year:1996
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Peer Reviewed:True
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Source Full Name:Applied Occupational and Environmental Hygiene
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Main Document Checksum:urn:sha-512:00c38ac90d1e67dce645ff76e50fdb5c2d05cb1f26e67d8c8f71638702bf1ed9cf1e4bac5d22bcc479663d7e2d159477b4c585b74eff206fd44652f522477f38
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