Trifilo Matthew J, Lane Thomas E
Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697-3900, USA.
J Neurovirol. 2003 Jun;9(3):315-24. doi: 10.1080/13550280390201029.
In the present study, the authors evaluated the contributions of the CXC chemokine ligand (CXCL)10 to leukocyte recruitment into the central nervous system (CNS) and disease development. Instillation of a replication-deficient adenovirus that expresses CXCL10 (AdCXCL10) into the CNS of C57BL/6 mice resulted in a rapid (day 3) and prolonged (day 21) infiltration of both CD4(+) and CD8(+) T cells as compared to mice infected with an adenovirus vector containing beta-galactosidase (Adbetagal). Despite increased T-cell infiltration into the CNS of AdCXCL10-infected mice, production of proinflammatory chemokines normally associated with the recruitment of activated T cells into the CNS was muted and mice developed limited neuropathology. Therefore, these results indicate that T-cell infiltration in the absence of appropriate activation is not sufficient to induce pathology within the CNS and that additional signals other than CXCL10 are required for induction of an immune-mediated neurologic disease.
在本研究中，作者评估了CXC趋化因子配体（CXCL）10在白细胞募集进入中枢神经系统（CNS）及疾病发展过程中的作用。将表达CXCL10的复制缺陷型腺病毒（AdCXCL10）注入C57BL/6小鼠的中枢神经系统，与感染含β-半乳糖苷酶腺病毒载体（Adbetagal）的小鼠相比，可导致CD4(+)和CD8(+) T细胞迅速（第3天）且持续（第21天）浸润。尽管AdCXCL10感染小鼠的中枢神经系统中有更多T细胞浸润，但通常与活化T细胞募集进入中枢神经系统相关的促炎趋化因子的产生受到抑制，且小鼠出现的神经病理学变化有限。因此，这些结果表明，在缺乏适当活化的情况下，T细胞浸润不足以在中枢神经系统内诱发病变，并且诱导免疫介导的神经疾病需要CXCL10以外的其他信号。
