Gonzalez Rafael, Glaser Janette, Liu Michael T, Lane Thomas E, Keirstead Hans S
Reeve-Irvine Research Center, Department of Anatomy and Neurobiology, University of California at Irvine,2111 Gillespie Neuroscience Research Facility, Irvine, CA 92697-4292, USA.
Exp Neurol. 2003 Nov;184(1):456-63. doi: 10.1016/s0014-4886(03)00257-7.
Injury to the spinal cord is followed by degeneration, which leads to progressive tissue loss and usually cystic cavitation. Cellular and humoral immune responses have been implicated as mediators of secondary degeneration, and the expression of leukocyte chemoattractants has been shown to precede immune cell influx. However, the relationship between the increased expression of chemoattractants, the invasion of lymphocytes, and overall lesion evolution is poorly understood. Here, we show that the T-lymphocyte chemoattractant CXCL10 is upregulated after dorsal hemisection injury to the adult mammalian spinal cord of C57/BL6 mice, and that antibody neutralization of CXCL10 beginning 1 day prior to injury dramatically reduces the T-lymphocyte invasion that normally occurs after trauma. Notably, this treatment resulted in a significant reduction of secondary tissue loss and functional deficit. We conclude that CXCL10 plays a critical role in recruitment of T lymphocytes to sites of spinal cord injury, and that a reduction of T-lymphocyte recruitment significantly enhances tissue preservation and functional outcome.
脊髓损伤后会发生变性，这会导致组织逐渐丧失，通常还会出现囊性空洞。细胞免疫和体液免疫反应被认为是继发性变性的介质，白细胞趋化因子的表达已被证明先于免疫细胞流入。然而，趋化因子表达增加、淋巴细胞浸润与整体损伤演变之间的关系尚不清楚。在此，我们表明，成年C57/BL6小鼠的脊髓背侧半切损伤后，T淋巴细胞趋化因子CXCL10上调，并且在损伤前1天开始对CXCL10进行抗体中和可显著减少创伤后正常发生的T淋巴细胞浸润。值得注意的是，这种治疗显著减少了继发性组织损失和功能缺陷。我们得出结论，CXCL10在将T淋巴细胞募集到脊髓损伤部位中起关键作用，减少T淋巴细胞募集可显著增强组织保存和功能结果。
