Pacheco Y, Dubois M, Prigent A F, Fonlupt P, Timouyasse L, Rey C, Chambe M T, Biot N, Perrin-Fayolle M, Pacheco H
Clin Chim Acta. 1987 Mar 30;163(3):267-77. doi: 10.1016/0009-8981(87)90245-2.
Among the various hypotheses proposed to explain immune cell defect in sarcoidosis, we examined thoroughly that of Faguet who described abnormalities of signal transmission at lymphocyte membrane level. Phosphatidylethanolamine methyltransferase and cAMP cGMP phosphodiesterases were studied in blood lymphocytes and monocytes from 8 subjects with sarcoidosis disease. Phosphatidylethanolamine methyltransferase (PMT1) plays an important regulatory role in membrane signal transmission. cAMP and cGMP phosphodiesterases (PDE) regulate cytoplasmic cyclic nucleotide levels and so participate in the modulation of the cell cycle. We observed a decreased PMT1 activity in lymphocytes and monocytes and a decreased cAMP and cGMP PDE activities in monocytes. It is not now possible to say if these abnormalities are primary or secondary. Whatever the origin of this dysfunctioning, these results evoke simultaneous disturbances of membrane signal transmission and cell cycle in monocytes and membrane abnormalities in lymphocytes. These abnormalities could explain some immune cell defects in sarcoidosis disease.
在为解释结节病中免疫细胞缺陷而提出的各种假说中,我们深入研究了法盖提出的假说,他描述了淋巴细胞膜水平信号传递的异常。我们对8名结节病患者血液中的淋巴细胞和单核细胞中的磷脂酰乙醇胺甲基转移酶以及环磷酸腺苷 - 环磷酸鸟苷磷酸二酯酶进行了研究。磷脂酰乙醇胺甲基转移酶(PMT1)在膜信号传递中起重要调节作用。环磷酸腺苷和环磷酸鸟苷磷酸二酯酶(PDE)调节细胞质中环状核苷酸的水平,从而参与细胞周期的调节。我们观察到淋巴细胞和单核细胞中PMT1活性降低,单核细胞中环磷酸腺苷和环磷酸鸟苷磷酸二酯酶活性降低。目前尚无法确定这些异常是原发性的还是继发性的。无论这种功能失调的起源如何,这些结果提示单核细胞中膜信号传递和细胞周期同时受到干扰,淋巴细胞中存在膜异常。这些异常可能解释结节病中的一些免疫细胞缺陷。