Nitta K, Uchida K, Miwa N, Kawashima A, Yumura W, Nihei H
Department of Medicine, Kidney Center, Tokyo Women's Medical College, Japan.
Endocr J. 1995 Jun;42(3):361-6. doi: 10.1507/endocrj.42.361.
Adhesion of lymphocytes to glomerular endothelial cells might be a critical step in the development of acute and chronic glomerulonephritis. The protective effect of anti-CD11a and anti-intercellular adhesion molecule (ICAM-1) antibodies on the cytotoxity elicited by phorbol 12-myristate 13-acetate (PMA)-stimulated lymphocytes was investigated by using cultured bovine glomerular endothelial cells (GEN). Both anti-CD11a and CD18 antibodies inhibited GEN injury induced by the activated lymphocytes in a dose-dependent manner. In addition, both antibodies also inhibited the adhesion of the activated lymphocytes to the GEN monolayers. These results suggest that it is important for activated lymphocytes to bind to GEN via adhesion molecules for cytotoxity to be produced by the activated lymphocytes.
淋巴细胞与肾小球内皮细胞的黏附可能是急性和慢性肾小球肾炎发生发展中的关键步骤。通过使用培养的牛肾小球内皮细胞（GEN），研究了抗CD11a和抗细胞间黏附分子（ICAM-1）抗体对佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）刺激的淋巴细胞引发的细胞毒性的保护作用。抗CD11a和CD18抗体均以剂量依赖性方式抑制活化淋巴细胞诱导的GEN损伤。此外，两种抗体还抑制活化淋巴细胞与GEN单层的黏附。这些结果表明，活化淋巴细胞通过黏附分子与GEN结合对于活化淋巴细胞产生细胞毒性很重要。
