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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Identification of C1q as the heat-labile serum cofactor required for immune complexes to stimulate endothelial expression of the adhesion molecules E-selectin and intercellular and vascular cell adhesion molecules 1
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Identification of C1q as the heat-labile serum cofactor required for immune complexes to stimulate endothelial expression of the adhesion molecules E-selectin and intercellular and vascular cell adhesion molecules 1

机译：将C1q鉴定为免疫复合物刺激粘附分子E-选择素和细胞间和血管细胞粘附分子的内皮表达所需的热不稳定血清辅因子1

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摘要

To examine the role of complement components as regulators of the expression of endothelial adhesive molecules in response to immune complexes (ICs), we determined whether ICs stimulate both endothelial adhesiveness for leukocytes and expression of E-selectin and intercellular and vascular cell adhesion molecules 1 (ICAM-1 and VCAM-1). We found that ICs [bovine serum albumin (BSA)-anti-BSA] stimulated endothelial cell adhesiveness for added leukocytes in the presence of complement-sufficient normal human serum (NHS) but not in the presence of heat-inactivated serum (HIS) or in tissue culture medium alone. Depletion of complement component C3 or C8 from serum did not prevent enhanced endothelial adhesiveness stimulated by ICs. In contrast, depletion of complement component C1q markedly inhibited IC-stimulated endothelial adhesiveness for leukocytes. When the heat-labile complement component C1q was added to HIS, the capacity of ICs to stimulate endothelial adhesiveness for leukocytes was completely restored. Further evidence for the possible role of C1q in mediating the effect of ICs on endothelial cells was the discovery of the presence of the 100- to 126-kDa C1q-binding protein on the surface of endothelial cells (by cytof luorogra-phy) and of message for the 33-kDa Clq receptor in resting endothelial cells (by reverse transcription-PCR). Inhibition of protein synthesis by cycloheximide blocked endothelial adhesiveness for leukocytes stimulated by either interleukin 1 or ICs in the presence of NHS. After stimulation with ICs in the presence of NHS, endothelial cells expressed increased numbers of adhesion molecules (E-selectin, ICAM-1, and VCAM-1). Endothelial expression of adhesion molecules mediated, at least in part, endothelial adhesiveness for leukocytes, since leukocyte adhesion was blocked by monoclonal antibodies directed against E-selectin. These studies show that ICs stimulate endothelial cells to express adhesive proteins for leukocytes in the presence of a heat-labile serum factor. That factor appears to be C1q.
机译：为了检查补体成分作为免疫复合物（IC）响应内皮粘附分子表达调节剂的作用，我们确定了IC是否同时刺激白细胞的内皮粘附性以及E-选择素和细胞间和血管细胞粘附分子的表达1（ ICAM-1和VCAM-1）。我们发现ICs [牛血清白蛋白（BSA）-抗BSA]在补体充足的正常人血清（NHS）的存在下刺激添加的白细胞对内皮细胞的粘附，但在热灭活的血清（HIS）或存在的情况下则没有。仅在组织培养基中。血清中补体成分C3或C8的耗竭并未阻止ICs刺激的内皮粘附性增强。相反，补体成分C1q的耗竭明显抑制了IC刺激的白细胞内皮粘附。当将热不稳定的补体成分C1q添加到HIS中时，IC刺激白细胞的内皮粘附能力完全恢复。 C1q在介导IC对内皮细胞作用中可能发挥作用的进一步证据是发现内皮细胞表面存在100-126 kDa C1q结合蛋白（通过细胞荧光法），并且静息内皮细胞中33 kDa Clq受体的信息（通过逆转录PCR）。在NHS存在下，环己酰亚胺对蛋白质合成的抑制作用阻断了白介素1或ICs刺激的白细胞的内皮粘附。在NHS存在下用IC刺激后，内皮细胞表达的粘附分子（E-选择素，ICAM-1和VCAM-1）数量增加。粘附分子的内皮表达至少部分地介导了白细胞的内皮粘附性，因为白细胞粘附被针对E-选择素的单克隆抗体所阻断。这些研究表明，IC在存在不稳定的血清因子的情况下刺激内皮细胞表达白细胞粘附蛋白。该因素似乎是C1q。

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