Cross Anne H, Ramsbottom Michael J, Lyons Jeri-Anne
Department of Neurology and Neurosurgery, Washington University School of Medicine, St. Louis, MO 63110, USA.
J Neuroimmunol. 2006 Apr;173(1-2):79-86. doi: 10.1016/j.jneuroim.2005.11.022. Epub 2006 Jan 30.
Inducible nitric oxide synthase (NOS2) expression in the central nervous system correlates with EAE disease activity. Inhibition of NOS2 ameliorates adoptively transferred EAE, yet exacerbates actively induced EAE. Herein, the encephalitogenicity of T cells induced by immunization in the presence or absence of NOS2 was examined. Upon passive transfer, T cells from myelin oligodendrocyte glycoprotein-immunized NOS2-deficient C57BL/6 mice induced more severe EAE than T cells from wild-type mice. The heightened encephalitogenicity of NOS2-/- T cells correlated with enhanced expression of VLA-4 (CD49d) and increased production of interferon gamma and tumor necrosis factor. NO plays an important regulatory role in autoimmune T cell induction.
中枢神经系统中诱导型一氧化氮合酶（NOS2）的表达与实验性自身免疫性脑脊髓炎（EAE）疾病活动相关。抑制NOS2可改善过继转移的EAE，但会加重主动诱导的EAE。在此，研究了在存在或不存在NOS2的情况下免疫诱导的T细胞的致脑炎性。被动转移时，来自用髓鞘少突胶质细胞糖蛋白免疫的NOS2缺陷型C57BL/6小鼠的T细胞比来自野生型小鼠的T细胞诱导更严重的EAE。NOS2基因敲除T细胞增强的致脑炎性与VLA-4（CD49d）表达增强以及干扰素γ和肿瘤坏死因子产生增加相关。NO在自身免疫性T细胞诱导中起重要调节作用。
