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,
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Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV 26505;
Division of Environmental and Occupational Health Sciences, Department of Medicine, National Jewish Medical and Research Center, Denver, CO 80206; and
Division of Pulmonary Science and Critical Care Medicine, Departments of Medicine and Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, CO 80206
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-
, and TNF-
, 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-, and TNF-;
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.
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