Interactions between fibroblastic reticular cells and B cells promote mesenteric lymph node lymphangiogenesis.

Détails

Ressource 1Télécharger: s41467-017-00504-9.pdf (10501.25 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_DE11D4AF0AD2
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Interactions between fibroblastic reticular cells and B cells promote mesenteric lymph node lymphangiogenesis.
Périodique
Nature communications
Auteur(s)
Dubey L.K., Karempudi P., Luther S.A., Ludewig B., Harris N.L.
ISSN
2041-1723 (Electronic)
ISSN-L
2041-1723
Statut éditorial
Publié
Date de publication
28/08/2017
Peer-reviewed
Oui
Volume
8
Numéro
1
Pages
367
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Résumé
Lymphatic growth (lymphangiogenesis) within lymph nodes functions to promote dendritic cell entry and effector lymphocyte egress in response to infection or inflammation. Here we demonstrate a crucial role for lymphotoxin-beta receptor (LTβR) signaling to fibroblastic reticular cells (FRCs) by lymphotoxin-expressing B cells in driving mesenteric lymph node lymphangiogenesis following helminth infection. LTβR ligation on fibroblastic reticular cells leads to the production of B-cell-activating factor (BAFF), which synergized with interleukin-4 (IL-4) to promote the production of the lymphangiogenic factors, vascular endothelial growth factors (VEGF)-A and VEGF-C, by B cells. In addition, the BAFF-IL-4 synergy augments expression of lymphotoxin by antigen-activated B cells, promoting further B cell-fibroblastic reticular cell interactions. These results underlie the importance of lymphotoxin-dependent B cell-FRC cross talk in driving the expansion of lymphatic networks that function to promote and maintain immune responsiveness.The growth of lymph nodes in response to infection requires lymphangiogenesis. Dubey et al. show that the mesenteric lymph node lymphangiogenesis upon helminth infection depends on the signaling loop between the B and fibroblastic reticular cells (FRCs), whereby the FRCs respond to lymphotoxin secreted by B cells by releasing B cell activating factor.

Mots-clé
Adaptive Immunity, Animals, B-Lymphocytes/physiology, Cytokines/metabolism, Cytokines/physiology, Helminthiasis/immunology, Helminthiasis/pathology, Lymph Nodes/immunology, Lymph Nodes/physiopathology, Lymphangiogenesis, Lymphatic Vessels/immunology, Lymphatic Vessels/pathology, Lymphatic Vessels/physiology, Mesentery/immunology, Mesentery/pathology, Mice, Mice, Inbred C57BL, Models, Immunological, Reticulin/physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
12/09/2017 12:56
Dernière modification de la notice
20/08/2019 16:02
Données d'usage