Eriksson H, Sjögren H O
Department of Tumor Immunology, Wallenberg Laboratory, Lund University, Sweden.
Immunology. 1995 Oct;86(2):304-10.
The major histocompatibility complex (MHC) class I molecules have been shown to be substrates to both of the complement C1 esterases. The effect of a C1 esterase-mediated cleavage of the MHC class I molecules on the activation process of lymphocytes was investigated by including the complement C1 esterase inhibitor (C1-Inh) in the medium during activation of human peripheral lymphocytes by staphylococcal enterotoxin A (SEA). The C1-Inh was shown to inhibit the activation of both CD4+ and CD8+ cells. No effect on activation of B lymphocytes was recorded, although the complement C1 complex was shown to bind to the B lymphocytes. Furthermore, the C1 complex bound to mononuclear cells was shown to be cleaved into molecular weights corresponding to the activated forms of the C1 esterases. The effect of the C1-Inh was much more pronounced at low cell density and the inhibition was not affected by the addition of interleukin-2 (IL-2). However, the inhibition was reduced when the cells were disturbed by addition of new portions of C1-Inh, 24 and 48 hr after the initiation of the activation. This indicates that the C1-Inh interference with the activation of T lymphocytes is mediated through a mechanism that requires some form of cell contact.
主要组织相容性复合体（MHC）I类分子已被证明是两种补体C1酯酶的作用底物。在通过金黄色葡萄球菌肠毒素A（SEA）激活人外周淋巴细胞的过程中，将补体C1酯酶抑制剂（C1-Inh）加入培养基中，研究了C1酯酶介导的MHC I类分子裂解对淋巴细胞激活过程的影响。结果显示，C1-Inh可抑制CD4 +和CD8 +细胞的激活。尽管补体C1复合物已被证明可与B淋巴细胞结合，但未观察到对B淋巴细胞激活有影响。此外，与单核细胞结合的C1复合物被裂解成与C1酯酶激活形式相对应的分子量。C1-Inh的作用在低细胞密度时更为明显，且这种抑制作用不受白细胞介素-2（IL-2）添加的影响。然而，在激活开始24小时和48小时后，当加入新的C1-Inh使细胞受到干扰时，抑制作用减弱。这表明C1-Inh对T淋巴细胞激活的干扰是通过一种需要某种形式细胞接触的机制介导的。
