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Partial IL-10 inhibition of the cell-mediated immune response in chronic beryllium disease.

Authors
Tinkle-SS; Kittle-LA; Newman-LS
Source
J Immunol 1999 Sep; 163(5):2747-2753
NIOSHTIC No.
20025376
Abstract
Chronic beryllium disease (CBD) provides a human disorder in which to study the delayed type IV hypersensitivity response to persistent Ag that leads to noncaseating pulmonary granuloma formation. We hypothesized that, in CBD, failure of IL-10 to modulate the beryllium-specific, cell-mediated immune response would result in persistent, maximal cytokine production and T lymphocyte proliferation, thus contributing to the development of granulomatous lung disease. To test this hypothesis, we used bronchoalveolar lavage cells from control and CBD subjects to evaluate the beryllium salt-specific production of endogenous IL-10 and the effects of exogenous human rIL-10 (rhIL-10) on HLA expression, on the production of IL-2, IFN-gamma, and TNF-alpha, and on T lymphocyte proliferation. Our data demonstrate that beryllium-stimulated bronchoalveolar lavage cells produce IL-10, and the neutralization of endogenous IL-10 does not increase significantly cytokine production, HLA expression, or T lymphocyte proliferation. Second, the addition of excess exogenous rhIL-10 partially inhibited the beryllium-stimulated production of IL-2, IFN-gamma, and TNF-alpha; however, we measured no change in T lymphocyte proliferation or in the percentage of alveolar macrophages expressing HLA-DP. Interestingly, beryllium salts interfered with an IL-10-stimulated decrease in the percentage of alveolar macrophages expressing HLA-DR. We conclude that, in the CBD-derived, beryllium-stimulated cell-mediated immune response, low levels of endogenous IL-10 have no appreciable effect; exogenous rhIL-10 has a limited effect on cytokine production and no effect on T lymphocyte proliferation or HLA expression.
Keywords
Immune-reaction; Beryllium-disease; Hypersensitivity; Immune-system-disorders; Pulmonary-system-disorders; Respiratory-system-disorders; Lung-disease
Contact
Dr. Sally S. Tinkle, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505
CODEN
JOIMA3
CAS No.
7440-22-4
Publication Date
19990901
Document Type
Journal Article
Email Address
sft3@cdc.gov
Fiscal Year
1999
NTIS Accession No.
NTIS Price
Issue of Publication
5
ISSN
0022-1767
NIOSH Division
HELD
Source Name
The Journal of Immunology
State
WV; CO
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