RESUMO

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 (T_H)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 T_H1 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 T_H1- nor T_H2-dependent IgG subclass-secreting cells were selectively enhanced. Our findings suggest that T_H1 activation alone does not account for increased production of IgG in experimental silicosis.