Tsunoda Ikuo, Kuang Li-Qing, Igenge Isaac Z M, Fujinami Robert S
Department of Neurology, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132-2305, USA.
J Neuroimmunol. 2005 Mar;160(1-2):122-34. doi: 10.1016/j.jneuroim.2004.11.007. Epub 2004 Dec 29.
We induced experimental allergic encephalomyelitis (EAE) in SJL/J mice, an animal model for multiple sclerosis (MS), using myelin oligodendrocyte glycoprotein (MOG)(92-106) peptide, following ultraviolet (UV) irradiation. While all control mice developed relapsing-remitting (RR)-EAE, UV irradiation induced secondary progressive (SP)-EAE in some of the mice. Although mild demyelination was observed with T cell infiltration in RR-EAE, large demyelinating lesions developed in SP-EAE with massive macrophage and neutrophil infiltration and immunoglobulin deposition, but with little T cell infiltration. UV irradiation induced higher anti-MOG antibody responses. In SP-EAE, lymphoproliferative responses and interferon-gamma production were decreased without alteration of interleukin-4.
我们使用髓鞘少突胶质细胞糖蛋白（MOG）（92 - 106）肽，在紫外线（UV）照射后，在SJL/J小鼠（一种多发性硬化症（MS）动物模型）中诱导实验性自身免疫性脑脊髓炎（EAE）。虽然所有对照小鼠都发生了复发缓解型（RR）-EAE，但紫外线照射在一些小鼠中诱导了继发进展型（SP）-EAE。虽然在RR-EAE中观察到伴有T细胞浸润的轻度脱髓鞘，但在SP-EAE中出现了大的脱髓鞘病变，伴有大量巨噬细胞和中性粒细胞浸润以及免疫球蛋白沉积，但T细胞浸润很少。紫外线照射诱导了更高的抗MOG抗体反应。在SP-EAE中，淋巴细胞增殖反应和干扰素-γ产生减少，而白细胞介素-4没有改变。
