Cutting edge: JAM-C controls homeostatic chemokine secretion in lymph node fibroblastic reticular cells expressing thrombomodulin

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...

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Bibliographic Details
Published in:	The Journal of immunology (1950) Vol. 187; no. 2; pp. 603 - 607
Main Authors:	Frontera, Vincent, Arcangeli, Marie-Laure, Zimmerli, Claudia, Bardin, Florence, Obrados, Elodie, Audebert, Stéphane, Bajenoff, Marc, Borg, Jean-Paul, Aurrand-Lions, Michel
Format:	Journal Article
Language:	English
Published:	United States 15-07-2011
Subjects:	Animals Cell Adhesion Molecules - biosynthesis Cell Adhesion Molecules - deficiency Cell Adhesion Molecules - physiology Cell Line, Transformed Cell Movement - genetics Cell Movement - immunology Chemokines - secretion Fibroblasts - immunology Fibroblasts - metabolism Fibroblasts - secretion Gene Expression Regulation - immunology HEK293 Cells Homeostasis - genetics Homeostasis - immunology Humans Immunoglobulins - biosynthesis Immunoglobulins - deficiency Immunoglobulins - physiology Lymph Nodes - cytology Lymph Nodes - immunology Lymph Nodes - secretion Male Mice Mice, 129 Strain Mice, Inbred C57BL Mice, Knockout Rats Rats, Inbred F344 Stromal Cells - immunology Stromal Cells - metabolism Thrombomodulin - biosynthesis
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Summary:	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 α 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 1α (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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1
ISSN:	0022-1767 1550-6606
DOI:	10.4049/jimmunol.1003441