Crane Isabel J, Xu Heping, Manivannan Ayyakkannu, McKillop-Smith Susan, Lamont Graeme, Wallace Carol, Liversidge Janet, Sharp Peter F, Forrester John V
Department of Ophthalmology, University of Aberdeen Medical School, Foresterhill, Aberdeen, GB.
Eur J Immunol. 2003 Feb;33(2):402-10. doi: 10.1002/immu.200310014.
This study has enabled us to identify the influence of the chemokine, macrophage inflammatory protein-1alpha (MIP-1alpha), on leukocyte behavior at the blood-retina barrier in vivo and its link with the inflammatory process and disease pathogenesis. MIP-1alpha has not previously been thought to be effective under conditions of physiological shear flow. However, short-term anti-MIP-1alpha treatment inhibited leukocyte slowing and accumulation and subsequent extravasation of leukocytes at the blood-retina barrier in animals with experimental autoimmune uveoretinitis. This was effective predominantly in the post-capillary venules which have been shown to be the main site of passage of leukocytes across the blood-retina barrier. Long-term anti-MIP-1alpha treatment also prevented decreased leukocyte velocity and reduced disease severity as measured clinically, histologically and in terms of blood-retina barrier breakdown.
这项研究使我们能够确定趋化因子巨噬细胞炎性蛋白-1α（MIP-1α）对体内血视网膜屏障处白细胞行为的影响，以及它与炎症过程和疾病发病机制的联系。以前认为MIP-1α在生理剪切流条件下无效。然而，在患有实验性自身免疫性葡萄膜视网膜炎的动物中，短期抗MIP-1α治疗可抑制白细胞在血视网膜屏障处的减慢、聚集以及随后的白细胞外渗。这主要在毛细血管后微静脉中有效，而毛细血管后微静脉已被证明是白细胞穿过血视网膜屏障的主要部位。长期抗MIP-1α治疗还可防止白细胞速度降低，并减轻临床、组织学以及血视网膜屏障破坏方面所测量的疾病严重程度。
