McCarron R M, Spatz M, Kempski O, Hogan R N, Muehl L, McFarlin D E
J Immunol. 1986 Dec 1;137(11):3428-35.
Lymph node cells from SJL mice immunized with guinea pig myelin basic protein proliferate in vitro to the same antigen. This proliferative response is abolished by depletion of macrophages-monocytes, but can be reconstituted by the addition of cerebral vascular endothelial cells (EC) freshly isolated from syngeneic mice with adoptively transferred acute experimental allergic encephalomyelitis (EAE). Reconstitution by EC from mice with EAE can be blocked by pretreatment of EC with syngeneic anti-I-A antisera. Freshly isolated EC from normal syngeneic mice do not restore responsiveness, but can be induced to present antigen by culture with murine recombinant immune interferon-gamma or supernatants from a variety of immune cell cultures. These findings are consistent with the hypothesis that immune cells release interferon and/or other soluble factors which induce I-A molecules on EC, which subsequently acquire the capacity to present antigen. The implications of these findings relate to the migration of cells across the blood-brain-barrier into the central nervous system, and are of importance in the understanding of the pathogenesis of several neurologic disorders.
用豚鼠髓鞘碱性蛋白免疫的SJL小鼠的淋巴结细胞在体外对相同抗原发生增殖反应。巨噬细胞-单核细胞的清除可消除这种增殖反应,但通过添加从同基因小鼠新鲜分离的脑血管内皮细胞(EC)并过继转移急性实验性变应性脑脊髓炎(EAE)可使其恢复。来自患有EAE小鼠的EC的重建可被用同基因抗I-A抗血清预处理EC所阻断。来自正常同基因小鼠的新鲜分离的EC不能恢复反应性,但通过与鼠重组免疫干扰素-γ或来自多种免疫细胞培养物的上清液培养可诱导其呈递抗原。这些发现与以下假说一致:免疫细胞释放干扰素和/或其他可溶性因子,这些因子诱导EC上的I-A分子,随后EC获得呈递抗原的能力。这些发现的意义涉及细胞穿过血脑屏障迁移到中枢神经系统,并且在理解几种神经系统疾病的发病机制中具有重要意义。