Publication

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

Journal Paper/Review - Aug 28, 2017

Units
PubMed
Doi

Citation
Dubey L, Karempudi P, Luther S, Ludewig B, Harris N. Interactions between fibroblastic reticular cells and B cells promote mesenteric lymph node lymphangiogenesis. Nat Commun 2017; 8:367.
Type
Journal Paper/Review (English)
Journal
Nat Commun 2017; 8
Publication Date
Aug 28, 2017
Issn Electronic
2041-1723
Pages
367
Brief description/objective

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.