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Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
Published on: June 13, 2014
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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
Summary
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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