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CCR7 调节淋巴细胞从腔室中迁出和再循环。

CCR7 regulates lymphocyte egress and recirculation through body cavities.

机构信息

Department of Tumor Genetics and Immunogenetics, Max-Delbrück-Center for Molecular Medicine, MDC, Berlin, Germany.

出版信息

J Leukoc Biol. 2010 Apr;87(4):671-82. doi: 10.1189/jlb.0709505. Epub 2009 Dec 22.

Abstract

T and B lymphocytes recirculate among blood, lymph, and extralymphoid tissues to ensure immune surveillance and the establishment of self-tolerance. The underlying mechanisms regulating homeostatic lymphocyte recirculation through body cavities are not fully understood. Here, we demonstrate that the homeostatic chemokine receptor CCR7 regulates homeostatic recirculation of lymphocytes through body cavities. CCR7 deficiency results in massive accumulation of CD4(+) and CD8(+) T cells and B-2 B cells in the peritoneal and pleural cavities. The increase in B-2 B and T lymphocytes is not associated with an altered maturation and/or activation status of these cells. Mechanistically, an increase in peritoneal lymphocyte numbers is caused by impaired egress of CCR7-deficient lymphocytes from body cavities. These results establish that CCR7 plays a crucial role in lymphocyte exit from the PerC.

摘要

T 和 B 淋巴细胞在血液、淋巴和淋巴外组织中循环,以确保免疫监视和自身耐受的建立。调节通过体腔的稳态淋巴细胞再循环的潜在机制尚未完全阐明。在这里,我们证明稳态趋化因子受体 CCR7 通过体腔调节淋巴细胞的稳态再循环。CCR7 缺陷导致腹腔和胸腔中大量的 CD4(+)和 CD8(+)T 细胞和 B-2 B 细胞积聚。B-2 B 和 T 淋巴细胞的增加与这些细胞的改变成熟和/或激活状态无关。从机制上讲,CCR7 缺陷淋巴细胞从体腔中排出受损导致腹腔淋巴细胞数量增加。这些结果表明 CCR7 在淋巴细胞从 PerC 中逸出过程中发挥着关键作用。

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