摘要Background: Chronic beryllium disease (CBD) develops in up to 16% of individuals exposed to beryllium and is characterized by granulomatous inflammation and the accumulation of T cells in the lung. Sensitization to beryllium (BeS) precedes CBD. We showed that alveolar macrophages (AMs) from CBD and BeS demonstrated significantly greater FcγRⅢ(CD16, encoded by the FCGR3A gene) phenotype than control. We hypothesized that these differences were related to polymorphisms in the FCGR3A gene, which has been associated with other autoimmune disorders, such as sarcoidosis and lupus, as well as protein levels.
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