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Journal of Environmental Pathology, Toxicology and Oncology
インパクトファクター: 1.241 5年インパクトファクター: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN 印刷: 0731-8898
ISSN オンライン: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v20.iSuppl.1.60
8 pages

IgG Subclass Responses in Experimental Silicosis

David N. Weissman
Health Effects Laboratory Division,National Institute for Occupational Safety and Health, Morgantown, WV
Ann F. Hubbs
National Institute for Occupational Safety and Health: Health Effects Laboratory Division, Morgantown,WV
Shu-Hai Huang
Guangxi Institute of Occupational Disease, Nanning, P.R. China
Charles F. Stanley
West Virginia University, Morgantown,WV
Yongyut Rojanasakul
West Virginia University Health Sciences Center, Department of Basic Pharmaceutical Sciences, Morgantown, WV 26506
Joseph K. H. Ma
West Virginia University, Morgantown,WV

要約

Silicosis is a crippling fibrotic lung disease induced by inhaling crystalline silica. In addition to fibrosis, silica inhalation by humans is associated with a number of immunological effects including increased levels of serum immunoglobulins (in particular IgG), increased prevalence of autoantibodies, and autoimmune disease. Recent studies using rodent models have shown that experimental silicosis is associated with a T-helper (TH)1 pattern of T-cell activation in the lungs and lung-associated lymph nodes after silica inhalation, which are also the sites of increased IgG production. We therefore hypothesized that the subclass distribution of IgG production occurring in experimental silicosis would suggest TH1 activation as the primary stimulus for IgG production. Using an ELISPOT assay, we found increased IgG-secreting spot-forming cells of all IgG subclasses in lungassociated lymph nodes taken from silica-exposed rats 3 to 4 months after aerosol exposure to silica.Neither TH1- nor TH2-dependent IgG subclass-secreting cells were selectively enhanced. Our findings suggest that TH1 activation alone does not account for increased production of IgG in experimental silicosis.