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

Lalit Kumar Dubey, Praneeth Karempudi, Sanjiv A. Luther, Burkhard Ludewig and Nicola L. Harris ()
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Lalit Kumar Dubey: Global Health Institute, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL)
Praneeth Karempudi: Global Health Institute, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL)
Sanjiv A. Luther: University of Lausanne
Burkhard Ludewig: Kantonsspital St. Gallen
Nicola L. Harris: Global Health Institute, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL)

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract 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.

Date: 2017
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DOI: 10.1038/s41467-017-00504-9

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