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A wide variety of exogenous or endogenous aggressors exhibit the capacity to induce pulmonary granulomatous lesions. This lesion is characterized by exacerbation of phagocytic function and tentative development of a specific immune response. In many clinical situations there is a well developed circulating antibody response with deficient cell-mediated immunity of variable degree. Finally, it is argued that the granulomatous lesion may be due to abnormal cooperation between T and B lymphocytes.
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