Wilcox C E, Healey D G, Baker D, Willoughby D A, Turk J L
Department of Experimental Pathology, St Bartholomew's Hospital Medical College, London U.K.
Immunology. 1989 Aug;67(4):435-40.
Previous studies have shown that endothelial cells in the central nervous system (CNS) of normal guinea-pigs constitutively express certain MHC class II determinants, whilst the expression of other determinants is apparent during the acute phase of chronic relapsing experimental allergic encephalomyelitis (CREAE). The expression of MHC class II determinants is retained by endothelial cells derived from normal guinea-pig brain tissue and maintained in culture. This present study demonstrates that the MHC class II molecules on these cells can be recognized by allogeneic lymphocytes, resulting in a proliferative response which is enhanced by the addition of exogenous IL-2. The endothelial cells were incapable of presenting either purified protein derivative or ovalbumin, but they could present autologous myelin basic protein (MBP), an encephalitogen implicated in the pathogenesis of EAE. The resulting lymphocyte proliferative response was of the same magnitude as that obtained when a control population of macrophages was used to present MBP. These results, therefore, suggest that cerebrovascular endothelia have the potential to play a role in the pathogenesis of EAE.
先前的研究表明,正常豚鼠中枢神经系统(CNS)中的内皮细胞组成性表达某些MHC II类决定簇,而其他决定簇的表达在慢性复发性实验性变应性脑脊髓炎(CREAE)的急性期明显。正常豚鼠脑组织来源的内皮细胞保留了MHC II类决定簇的表达并在培养中维持。本研究表明,这些细胞上的MHC II类分子可被同种异体淋巴细胞识别,导致增殖反应,添加外源性IL-2可增强该反应。内皮细胞无法呈递纯化蛋白衍生物或卵清蛋白,但它们可以呈递自身髓磷脂碱性蛋白(MBP),一种与实验性自身免疫性脑脊髓炎(EAE)发病机制有关的致脑炎因子。由此产生的淋巴细胞增殖反应与使用对照巨噬细胞群体呈递MBP时获得的反应强度相同。因此,这些结果表明脑血管内皮细胞有可能在EAE的发病机制中发挥作用。