Hughes C C, Male D K, Lantos P L
Department of Neuropathology, Institute of Psychiatry, London, U.K.
Immunology. 1988 Aug;64(4):677-81.
Although lymphocyte traffic through the brain is normally low, this can increase dramatically in response to infection or an autoimmune reaction. We have studied the adhesion of lymphocytes to cerebral endothelium in vitro in an attempt to model the first step of the infiltration process--that is, the initial interaction between the lymphocytes and endothelial cells--by brief co-culture of lymph node cells with monolayers of cultured cerebral endothelium. In this system we find that the basal level of adhesion can be increased in a dose-dependent manner by pre-treatment of the endothelial cells with interferon-gamma (IFN-gamma) and/or tumour necrosis factor (TNF) but not with interleukin-1 (IL-1). This increased adhesion can be blocked by incubating the IFN-gamma-treated cells with an antibody that is thought to bind to the common beta-chain of the lymphocyte functional antigen-1 (LFA-1) family of molecules. This suggests that endothelial cells express either LFA-1 or a molecule sharing the beta-subunit (of which several have been described) and furthermore that this molecule is involved in the regulation of lymphocyte traffic into the brain.
虽然淋巴细胞通过大脑的流量通常较低，但在感染或自身免疫反应时，这一流量会急剧增加。我们通过将淋巴结细胞与培养的脑内皮细胞单层进行短暂共培养，在体外研究淋巴细胞与脑内皮的黏附，试图模拟浸润过程的第一步，即淋巴细胞与内皮细胞之间的初始相互作用。在这个系统中，我们发现通过用γ干扰素（IFN-γ）和/或肿瘤坏死因子（TNF）预处理内皮细胞，而非白细胞介素-1（IL-1），可以使基础黏附水平呈剂量依赖性增加。通过用一种被认为能与淋巴细胞功能抗原-1（LFA-1）分子家族的共同β链结合的抗体孵育经IFN-γ处理的细胞，这种增加的黏附可以被阻断。这表明内皮细胞表达LFA-1或共享β亚基的分子（已经描述了几种），而且该分子参与调节淋巴细胞进入大脑的流量。
