Nature 子刊：“杀手”细胞摧毁重入淋巴结的枝状细胞
生物谷：树枝状细胞是一种特定的免疫细胞，研究人员在5月在线出版的《自然—免疫学》（Nature Immunology）期刊上报告说，一种武装起来的“杀手”细胞能够摧毁重新进入淋巴结中的枝状细胞。这种由特定抗原T细胞杀死的细胞的死亡，会减少其他未受影响的免疫细胞的激活，避免过度的免疫反应。新结果推翻了一种主导观点，即淋巴结能提供一种阻止活性T细胞进入的限制性环境。
效应器记忆 CD8+T细胞是一种免疫“杀手”细胞，Sallusto和同事发现，“休眠”的淋巴结能继续阻止以前激活的CD8+T细胞的进入。然而，当感染过程出现炎症信号时，淋巴结会被激活，表达出一种名为CXCL9的化学信号，召集记忆T细胞涌向血管。这些记忆细胞表达一种能识别CXCL9的受体CXCR3。
除了检查进一步的免疫活性外，CXCL9进入通道还提供了与病原菌如HIV作斗争的方法。新研究将有助于更有效的疫苗和免疫治疗方法的开发。（引自科学时报）
Nature Immunology
Published online: 27 May 2007 | doi:10.1038/ni1469
L-selectin-negative CCR7- effector and memory CD8+ T cells enter reactive lymph nodes and kill dendritic cells
Greta Guarda1, Miroslav Hons1, Silvia F Soriano2, Alex Y Huang3,4, Rosalind Polley3, Alfonso Martín-Fontecha1, Jens V Stein2, Ronald N Germain3, Antonio Lanzavecchia1 & Federica Sallusto1
Abstract
T lymphocytes lacking the lymph node–homing receptors L-selectin and CCR7 do not migrate to lymph nodes in the steady state. Instead, we found here that lymph nodes draining sites of mature dendritic cells or adjuvant inoculation recruited L-selectin-negative CCR7- effector and memory CD8+ T cells. This recruitment required CXCR3 expression on T cells and occurred through high endothelial venules in concert with lumenal expression of the CXCR3 ligand CXCL9. In reactive lymph nodes, recruited T cells established stable interactions with and killed antigen-bearing dendritic cells, limiting the ability of these dendritic cells to activate naive CD4+ and CD8+ T cells. The inducible recruitment of blood-borne effector and memory T cells to lymph nodes may represent a mechanism for terminating primary and limiting secondary immune responses.
- Institute for Research in Biomedicine, CH-6500 Bellinzona, Switzerland.
- Theodor Kocher Institute, University of Bern, CH-3012 Bern, Switzerland.
- National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
- Present address: Division of Pediatric Hematology/Oncology, Rainbow Babies & Children's Hospital, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
Correspondence to: Federica Sallusto1 e-mail: federica.sallusto@irb.unisi.ch
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