Whelan J P, Eriksson U, Lampson L A
J Immunol. 1986 Oct 15;137(8):2561-6.
Previous work indicates that the weak expression in neural tissues of beta 2-microglobulin (beta 2-m) and major histocompatibility complex (MHC) class I gene products can be increased experimentally. Physiologic conditions in which greater neural MHC expression occurs are not well defined. Here we have asked whether protection from blood-borne antigens afforded by the blood-brain barrier is related to the lack of MHC expression. A rabbit antiserum raised against purified mouse beta 2-m was used in an immunocytochemical assay. The serum reacted strongly with lymphoid tissues and was inhibited by purified beta 2-m. No beta 2-m was detected in neurons or glia in any brain area examined. A barrier-free region, the area postrema, showed the same lack of neural cell staining. Blood vessel walls in the same sections were beta 2-m+. It is unlikely that these staining patterns are due to cell type-specific beta 2-m degradation, since frozen and formaldehyde-perfused, paraffin-embedded preparations gave similar results. Failure to detect beta 2-m in the area postrema suggests that passive exposure to environmental antigens, immunomodulators, or immunocompetent cells is not sufficient to induce neural class I expression. Rather, if increased expression of beta 2-m and class I occurs in vivo, additional stimulus is required.
先前的研究表明，β2-微球蛋白（β2-m）和主要组织相容性复合体（MHC）I类基因产物在神经组织中的弱表达可通过实验增加。神经MHC表达增加时的生理条件尚未明确界定。在此，我们探讨血脑屏障对血源性抗原的保护作用是否与MHC表达缺失有关。在免疫细胞化学分析中，使用了针对纯化小鼠β2-m制备的兔抗血清。该血清与淋巴组织强烈反应，并被纯化的β2-m抑制。在所检查的任何脑区的神经元或神经胶质细胞中均未检测到β2-m。无屏障区域——最后区，也显示出相同的神经细胞无染色情况。同一切片中的血管壁β2-m呈阳性。这些染色模式不太可能是由于细胞类型特异性的β2-m降解所致，因为冷冻切片和甲醛灌注、石蜡包埋的标本给出了相似的结果。在最后区未检测到β2-m表明，被动暴露于环境抗原、免疫调节剂或免疫活性细胞不足以诱导神经I类表达。相反，如果β2-m和I类在体内表达增加，则需要额外的刺激。
