Department of Molecular Biology & Biochemistry, UC Irvine, CA 92697-3900, USA.
Virology. 2013 Jan 5;435(1):110-7. doi: 10.1016/j.virol.2012.08.049.
Inoculation with the neurotropic JHM strain of mouse hepatitis virus (MHV) into the central nervous system (CNS) of susceptible strains of mice results in an acute encephalomyelitis in which virus preferentially replicates within glial cells while excluding neurons. Control of viral replication during acute disease is mediated by infiltrating virus-specific T cells via cytokine secretion and cytolytic activity, however sterile immunity is not achieved and virus persists resulting in chronic neuroinflammation associated with demyelination. CXCR2 is a chemokine receptor that upon binding to specific ligands promotes host defense through recruitment of myeloid cells to the CNS as well as protecting oligodendroglia from cytokine-mediated death in response to MHV infection. These findings highlight growing evidence of the diverse and important role of CXCR2 in regulating neuroinflammatory diseases.
将神经嗜性 JHM 株小鼠肝炎病毒(MHV)接种到易感品系小鼠的中枢神经系统(CNS)中,会导致急性脑脊髓炎,其中病毒优先在神经胶质细胞内复制,而排除神经元。急性疾病期间病毒复制的控制是通过浸润的病毒特异性 T 细胞通过细胞因子分泌和细胞溶解活性介导的,但是没有达到无菌免疫,病毒持续存在导致与脱髓鞘相关的慢性神经炎症。CXCR2 是一种趋化因子受体,与特定配体结合后通过将髓样细胞募集到中枢神经系统来促进宿主防御,以及在 MHV 感染时保护少突胶质细胞免受细胞因子介导的死亡。这些发现强调了 CXCR2 在调节神经炎症性疾病中的多种重要作用的不断增加的证据。