Homing to central nervous system vasculature by antigen-specific lymphocytes. I. Localization of 14C-labeled cells during acute, chronic, and relapsing experimental allergic encephalomyelitis.

Homing to central nervous system vasculature by antigen-specific lymphocytes. I. Localization of 14C-labeled cells during acute, chronic, and relapsing experimental allergic encephalomyelitis.
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发表时间:
1990-08
期刊:
Laboratory investigation; a journal of technical methods and pathology
影响因子:
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通讯作者:
A. Cross;B. Cannella;C. Brosnan;C. S. Raine
A. Cross;B. Cannella;C. Brosnan;C. S. Raine
中科院分区:
其他
文献类型:
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作者:
A. Cross;B. Cannella;C. Brosnan;C. S. Raine

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[14C]胸腺嘧啶标记髓鞘碱性蛋白(MBP)致敏淋巴细胞从MBP免疫小鼠被动转移到幼稚的同基因受体诱导慢性复发实验性过敏性脑脊髓炎。在急慢性疾病和临床复发期间,标记淋巴细胞在中枢神经系统中被定位和定量。结果表明,mbp免疫T细胞在发病前24小时和发病期间(移植后5 - 7天)可返回中枢神经系统内皮。出乎意料的是,标记的mbp免疫细胞从未迁移到远离血管的地方,尽管存在大量实质炎症细胞浸润,但几乎总是停留在血管周围区域。定量显示,在急性和早期慢性疾病期间,标记细胞占炎性细胞的少数(通常为1%至4%)。此外,在临床复发时,标记细胞无法在中枢神经系统中显示。我们得出结论,在该模型中,mbp免疫淋巴细胞仅从血管周围位置起作用,以协调主要来自受体的炎症细胞的涌入。
Chronic relapsing experimental allergic encephalomyelitis was induced by the passive transfer of [14C]thymidine-labeled myelin basic protein (MBP)-sensitized lymphocytes from MBP-immunized mice to naive syngeneic recipients. Labeled lymphocytes were localized and quantitated in the central nervous system during acute and chronic disease and clinical relapses. The results have shown that MBP-immune T cells home to the central nervous system endothelium 24 hours prior to and during initial clinical disease (5 to 7 days posttransfer). Unexpectedly, labeled MBP-immune cells never migrated far from blood vessels and, despite the presence of massive parenchymal inflammatory cell infiltration, almost invariably remained within the perivascular area. Quantitation revealed that labeled cells represented a minority (usually 1% to 4%) of the inflammatory cells during acute and early chronic disease. Furthermore, labeled cells could not be demonstrated in the central nervous system at the time of clinical relapse. We conclude that in this model, MBP-immune lymphocytes act exclusively from a perivascular location to orchestrate the influx of inflammatory cells that are predominantly of recipient derivation.