[Expression of bc1-2 protein in collagen vascular diseases with pulmonary interstitial involvement]

Expression of bc1-2 protein was studied immunohistochemically in 25 patients with collagen vascular diseases and in 10 patients with idiopathic interstitial pneumonia. The collagen vascular diseases included rheumatoid arthritis (n = 9), progressive systemic sclerosis (n = 9), polymyositis/dermatomyositis (n = 4), Sjögren's syndrome (n = 2), and systemic lupus erythematosus (n = 1). All 35 patients underwent open lung biopsy; cellular infiltration, fibrosis, and lymphoid aggregation were scored according to Cherniack's classification. T lymphocytes (CD43: DFT-1) and B lymphocytes (CD20:L-26) were also evaluated. Expression of bc1-2 protein was dominant in T lymphocytes infiltrating the alveolar interstitium and in B lymphocytes in the mantle zone of lymphoid follicles. In collagen vascular diseases, the degree of expression of bc1-2 protein in those T lymphocytes was closely related to the alveolar lymphocyte infiltration score. However, these findings were not marked in the patients with idiopathic interstitial pneumonia, and were not related to the underlying disease in the patients with collagen vascular diseases. The expression of bc1-2 protein in T lymphocytes was not related to fibrosis or to lymphoid aggregation. Expression of bc1-2 protein in B lymphocytes did not correlate with pathological scores or with underlying disease. Bc1-2 protein has been recognized as an oncogene that suppresses apoptosis. Marked expression of bc1-2 protein in T lymphocytes from patients with collagen vascular diseases indicates that oversuppression of apoptosis may be related to the pathogenesis of pulmonary interstitial involvement in these conditions. Further clinicopathological studies focusing on apoptosis in collagen vascular diseases and in idiopathic interstitial pneumonia are needed.