Imhof B A, Dunon D
Department of Pathology, CMU, Geneva.
Horm Metab Res. 1997 Dec;29(12):614-21. doi: 10.1055/s-2007-979112.
Inflammation represents the consequence of capillary dilation with accumulation of fluid (edema) and the immigration of leukocytes. By the end of the last century, Metchnikoff noted the power of certain blood cells to move toward bacteria and foreign substances and ingest them. In fact, leukocytes adhere to the vascular endothelium, and subsequently leave the circulation by transendothelial migration driven by chemoattractants, a process known as diapedesis. Reversible adherence of leukocytes to endothelium, basement membranes, and other surfaces on which they crawl is an essential event in the establishment of inflammation, whose molecular basis is beginning to be understood. Inflammation can become chronic. The acute process, characterized by neutrophil infiltration and edema, gives way to a subsequent predominance of mononuclear phagocytes or lymphocytes. Insulin-dependent diabetes mellitus is the result of organ-specific autoimmune destruction of the insulin secreting beta-cells in the pancreatic islets of Langerhans. It has become evident that diabetes mellitus is a multifactorial disease caused in part by infiltrating T-lymphocytes, comparable to situations of inflammation. After presentation of the different effectors of the immune system and their fluxes through the body, this review will propose a general model of adhesion between leukocytes and endothelial cells. It will emphasize how the homing specificity of lymphocyte subsets to different lymphoid organs is ensured, and how leukocyte migration to sites of inflammation is regulated. Finally, general therapeutic perspectives based on adhesion molecules leading to cure or prevention of chronic inflammation will be discussed.
炎症表现为毛细血管扩张并伴有液体蓄积（水肿）以及白细胞移入的结果。在上个世纪末，梅契尼科夫注意到某些血细胞具有向细菌和异物移动并吞噬它们的能力。事实上，白细胞会黏附于血管内皮，随后在趋化因子的驱动下通过跨内皮迁移离开循环系统，这一过程称为血细胞渗出。白细胞与内皮、基底膜以及它们爬行的其他表面的可逆性黏附是炎症发生过程中的一个重要事件，其分子基础正逐渐被人们所理解。炎症可能会发展为慢性炎症。以中性粒细胞浸润和水肿为特征的急性过程会让位于随后单核吞噬细胞或淋巴细胞占主导的阶段。胰岛素依赖型糖尿病是由朗格汉斯胰岛中分泌胰岛素的β细胞发生器官特异性自身免疫破坏所致。很明显，糖尿病是一种多因素疾病，部分原因是浸润的T淋巴细胞，这与炎症情况类似。在介绍了免疫系统的不同效应器及其在体内的流动情况之后，本综述将提出白细胞与内皮细胞之间黏附的一般模型。它将强调淋巴细胞亚群对不同淋巴器官归巢特异性是如何得以确保的，以及白细胞向炎症部位迁移是如何被调控的。最后，将讨论基于黏附分子实现治愈或预防慢性炎症的一般治疗前景。
