Cutting Edge: JAM-C Controls Homeostatic Chemokine Secretion in Lymph Node Fibroblastic Reticular Cells Expressing Thrombomodulin

被引:14
作者
Frontera, Vincent [1 ,2 ,3 ]
Arcangeli, Marie-Laure [1 ,2 ,3 ]
Zimmerli, Claudia [4 ]
Bardin, Florence [1 ,2 ,3 ]
Obrados, Elodie [1 ,2 ,3 ]
Audebert, Stephane [1 ]
Bajenoff, Marc [5 ,6 ,7 ]
Borg, Jean-Paul [1 ,2 ,3 ]
Aurrand-Lions, Michel [1 ,2 ,3 ]
机构
[1] Ctr Rech Cancerol Marseille, INSERM, UMR891, F-13009 Marseille, France
[2] Inst J Paoli I Calmettes, F-13009 Marseille, France
[3] Univ Aix Marseille 2, F-13007 Marseille, France
[4] CMU, Dept Pathol & Immunol, CH-1204 Geneva, Switzerland
[5] Univ Aix Marseille 2, Ctr Immunol Marseille Luminy, F-13288 Marseille 09, France
[6] INSERM, UMR631, F-13288 Marseille 09, France
[7] CNRS, UMR 6102, F-13288 Marseille 09, France
基金
瑞士国家科学基金会;
关键词
MIGRATION; MOLECULE; INTEGRIN; EGRESS; ORGANS;
D O I
10.4049/jimmunol.1003441
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The development and maintenance of secondary lymphoid organs, such as lymph nodes, occur in a highly coordinated manner involving lymphoid chemokine production by stromal cells. Although developmental pathways inducing lymphoid chemokine production during organogenesis are known, signals maintaining cytokine production in adults are still elusive. In this study, we show that thrombomodulin and platelet-derived growth factor receptor a identify a population of fibroblastic reticular cells in which chemokine secretion is controlled by JAM-C. We demonstrate that Jam-C-deficient mice and mice treated with Ab against JAM-C present significant decreases in stromal cell-derived factor 1 alpha (CXCL12), CCL21, and CCL19 intranodal content. This effect is correlated with reduced naive T cell egress from lymph nodes of anti-JAM-C-treated mice. The Journal of Immunology, 2011, 187: 603-607.
引用
收藏
页码:603 / 607
页数:5
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