Experimental data already obtained in this project demonstrate a deficiency in the ability of unprimed lung tissue to manifest immune responses to local immunization in vivo and a reduced ability of pulmonary lymphoid cells to respond to immune stimulation in vitro. The overall objective of this research proposal is to elucidate the mechanisms responsible for the reduced responses of pulmonary lymphoid cells to immune stimulation in vivo and in vitro. The adequacy of the composition of pulmonary lymphoid cells will be defined by determining whether antigen-reactive B and T lymphocytes, appropriate for generation of anti-body-forming cells, are present normally in murine lungs and by determining whether murine alveolar macrophages are capable of processing antigen for immune responses. Suppressive factors which may be operative in the lung will be defined by determining the mechanism by which murine alveolar macrophages inhibit the generation of antibody-forming cells in vitro and the mechanism by which canine alveolar macrophages suppress lymphocyte responses to mitogens. The innate immune reactivity of pulmonary lymphocytes will be defined by determining whether the reduced proliferative responses of canine bronchoalveolar lymphocytes is due to abnormalities in immune recognition or abnormalities in proliferative events preceding DNA synthesis. These studies are expected to provide information which increases our understanding of factors regulating immune reactivity of normal lungs and may provide insight into factors contributing to the pathogenesis of immunologic lung disease.
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