In susceptible persons, beryllium exposure can lead to a cell-mediated immune response. The T-cells become sensitized to beryllium. Each subsequent exposure leads to an immune response involving CD4+ helper T-lymphocytes and macrophages accumulating in the lungs. As this response continues macrophages, CD+4 T-lymphocytes and plasma cells aggregate together to form the noncaseating granulomas. When beryllium is phagocytized by macrophages, the beryllium triggers macrophage apoptosis, thereby reducing beryllium clearance from the lungs and eventually resulting in secondary necrosis and lysis. Eventually, the outcome is fibrosis of the lung.
Several studies have shown that there is a genetic component to beryllium sensitivity. Specifically, those beryllium-exposed workers with a mutation at the HLA-DPB1 Glu position have increased prevalence of beryllium sensitization and chronic beryllium disease.  The HLA-DPB1 gene is important for MHC class II molecule function on antigen presenting cells. A study of the immune response to beryllium in individuals who express the HLA-DP2 allele found that CD4 T-cells do not detect the Be+ cation itself, but instead detect surface changes in the HLA-DP2/peptide complex in which Be+ is embedded. Those researchers concluded that chronic beryllium disease is a predisposition that lies between "allergic hypersensitivity and autoimmunity." 
According to the International Agency for Research on Cancer, beryllium and beryllium compounds are Category 1 carcinogens; they are carcinogenic to both animals and humans.