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Integrin-Alpha IIb Identifies Murine Lymph Node Lymphatic Endothelial Cells Responsive to RANKL

Olga G Cordeiro1, Mélanie Chypre1,2, Nathalie Brouard3

  • 1CNRS UPR 3572, University of Strasbourg, Laboratory of Immunopathology and Therapeutic Chemistry/ MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.

Plos One
|March 25, 2016
PubMed

Insights

Lymphatic endothelial cells (LECs) in lymph nodes express integrin alpha 2b (ITGA2b), regulated by stromal cell signals like RANKL and lymphotoxin-β. This reveals new insights into LEC activation and heterogeneity within secondary lymphoid organs.

Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • Lymphatic endothelial cells (LECs) exhibit heterogeneity influenced by microenvironmental signals.
  • LECs in secondary lymphoid organs encounter diverse cell types and immune stimuli.
  • The specific LEC activation signals and their sources in steady-state secondary lymphoid organs are not fully understood.

Purpose of the Study:

  • To investigate the expression of integrin alpha 2b (ITGA2b) on lymph node LECs.
  • To identify the signaling pathways and cell sources that regulate LEC activation and ITGA2b expression.
  • To understand the heterogeneity of LECs within the secondary lymphoid organ microenvironment.

Main Methods:

  • Immunohistochemistry to detect ITGA2b expression on LEC subsets in lymph nodes.
  • Analysis of ITGA2b expression changes in response to immunization.
  • Genetic manipulation of receptor activator of NF-κB ligand (RANKL) in stromal cells.
  • Assessment of lymphotoxin-β receptor (LTBR) signaling in LECs.

Main Results:

  • ITGA2b is expressed by a subset of lymph node LECs in medullary, cortical, and subcapsular sinuses, with specific localization patterns.
  • ITGA2b expression on LECs increases following immunization.
  • Stromal cell-derived RANKL and LTBR signaling regulate the proportion of ITGA2b+ LECs.
  • Lymph node LECs express RANK, unlike peripheral LECs.

Conclusions:

  • Stromal reticular cells activate LECs through RANKL, contributing to LEC heterogeneity.
  • Hematopoietic cell-derived lymphotoxin signaling also influences LEC activation.
  • These findings elucidate key mechanisms of LEC activation and regulation within the secondary lymphoid organ microenvironment.

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