Lee Woo-Yong, Kubes Paul
Department of Physiology and Biophysics, Immunology Research Group, Institute of Infection, Immunity and Inflammation, University of Calgary, Calgary, AB, Canada.
J Hepatol. 2008 Mar;48(3):504-12. doi: 10.1016/j.jhep.2007.12.005. Epub 2007 Dec 31.
It is well known that leukocyte recruitment is a multi-step cascade that requires an initial tethering to the endothelium of post-capillary venules followed by rolling along the vessel wall until appropriate activating molecules are encountered which cause firm adhesion and emigration out of the vasculature. Recruitment of leukocytes in the post-sinusoidal venules of the liver follows a similar paradigm. However, distinct from most other organs is the observation that many leukocytes can also be seen adhering in the sinusoids which are specialized hepatic capillaries. In this review, the lack of importance of rolling in sinusoids is discussed. The molecular mechanisms leading to adhesion in the liver sinusoids can occur via integrin-dependent as well as integrin-independent mechanisms. In addition to the "classical" beta(1)- and beta(2)-integrin adhesion, some of the "non-classical" (non-integrin dependent) pathways including CD44 and vascular adhesion protein-1, are discussed.
众所周知,白细胞募集是一个多步骤级联反应,首先需要与毛细血管后微静脉的内皮细胞进行初始拴系,随后沿血管壁滚动,直到遇到合适的激活分子,这些分子会导致牢固黏附并从血管系统中逸出。肝脏窦后微静脉中的白细胞募集遵循类似的模式。然而,与大多数其他器官不同的是,观察到许多白细胞也可黏附在作为特殊肝毛细血管的肝血窦中。在这篇综述中,讨论了肝血窦中滚动的不重要性。导致肝血窦黏附的分子机制可通过整合素依赖性以及整合素非依赖性机制发生。除了“经典的”β(1)和β(2)整合素黏附外,还讨论了一些“非经典的”(非整合素依赖性)途径,包括CD44和血管黏附蛋白-1。