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Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node
Lymph node (LN)-resident stromal cells play an essential role in the proper functioning of LNs. The stromal compartment of the LN undergoes significant compensatory changes to produce a milieu amenable for regulation of the immune response. We have identified a distinct population of leptin receptor...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8801441/ https://www.ncbi.nlm.nih.gov/pubmed/35111151 http://dx.doi.org/10.3389/fimmu.2021.730438 |
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author | Jiang, Liwei Yilmaz, Mine Uehara, Mayuko Cavazzoni, Cecilia B. Kasinath, Vivek Zhao, Jing Naini, Said Movahedi Li, Xiaofei Banouni, Naima Fiorina, Paolo Shin, Su Ryon Tullius, Stefan G. Bromberg, Jonathan S. Sage, Peter T. Abdi, Reza |
author_facet | Jiang, Liwei Yilmaz, Mine Uehara, Mayuko Cavazzoni, Cecilia B. Kasinath, Vivek Zhao, Jing Naini, Said Movahedi Li, Xiaofei Banouni, Naima Fiorina, Paolo Shin, Su Ryon Tullius, Stefan G. Bromberg, Jonathan S. Sage, Peter T. Abdi, Reza |
author_sort | Jiang, Liwei |
collection | PubMed |
description | Lymph node (LN)-resident stromal cells play an essential role in the proper functioning of LNs. The stromal compartment of the LN undergoes significant compensatory changes to produce a milieu amenable for regulation of the immune response. We have identified a distinct population of leptin receptor-expressing (LepR(+)) stromal cells, located in the vicinity of the high endothelial venules (HEVs) and lymphatics. These LepR(+) stromal cells expressed markers for fibroblastic reticular cells (FRCs), but they lacked markers for follicular dendritic cells (FDCs) and marginal reticular cells (MRCs). Leptin signaling deficiency led to heightened inflammatory responses within the LNs of db/db mice, leakiness of HEVs, and lymphatic fragmentation. Leptin signaling through the JAK/STAT pathway supported LN stromal cell survival and promoted the anti-inflammatory properties of these cells. Conditional knockout of the LepR(+) stromal cells in LNs resulted in HEV and extracellular matrix (ECM) abnormalities. Treatment of ob/ob mice with an agonist leptin fusion protein restored the microarchitecture of LNs, reduced intra-LN inflammatory responses, and corrected metabolic abnormalities. Future studies are needed to study the importance of LN stomal cell dysfunction to the pathogenesis of inflammatory responses in type 2 diabetes (T2D) in humans. |
format | Online Article Text |
id | pubmed-8801441 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-88014412022-02-01 Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node Jiang, Liwei Yilmaz, Mine Uehara, Mayuko Cavazzoni, Cecilia B. Kasinath, Vivek Zhao, Jing Naini, Said Movahedi Li, Xiaofei Banouni, Naima Fiorina, Paolo Shin, Su Ryon Tullius, Stefan G. Bromberg, Jonathan S. Sage, Peter T. Abdi, Reza Front Immunol Immunology Lymph node (LN)-resident stromal cells play an essential role in the proper functioning of LNs. The stromal compartment of the LN undergoes significant compensatory changes to produce a milieu amenable for regulation of the immune response. We have identified a distinct population of leptin receptor-expressing (LepR(+)) stromal cells, located in the vicinity of the high endothelial venules (HEVs) and lymphatics. These LepR(+) stromal cells expressed markers for fibroblastic reticular cells (FRCs), but they lacked markers for follicular dendritic cells (FDCs) and marginal reticular cells (MRCs). Leptin signaling deficiency led to heightened inflammatory responses within the LNs of db/db mice, leakiness of HEVs, and lymphatic fragmentation. Leptin signaling through the JAK/STAT pathway supported LN stromal cell survival and promoted the anti-inflammatory properties of these cells. Conditional knockout of the LepR(+) stromal cells in LNs resulted in HEV and extracellular matrix (ECM) abnormalities. Treatment of ob/ob mice with an agonist leptin fusion protein restored the microarchitecture of LNs, reduced intra-LN inflammatory responses, and corrected metabolic abnormalities. Future studies are needed to study the importance of LN stomal cell dysfunction to the pathogenesis of inflammatory responses in type 2 diabetes (T2D) in humans. Frontiers Media S.A. 2022-01-17 /pmc/articles/PMC8801441/ /pubmed/35111151 http://dx.doi.org/10.3389/fimmu.2021.730438 Text en Copyright © 2022 Jiang, Yilmaz, Uehara, Cavazzoni, Kasinath, Zhao, Naini, Li, Banouni, Fiorina, Shin, Tullius, Bromberg, Sage and Abdi https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Jiang, Liwei Yilmaz, Mine Uehara, Mayuko Cavazzoni, Cecilia B. Kasinath, Vivek Zhao, Jing Naini, Said Movahedi Li, Xiaofei Banouni, Naima Fiorina, Paolo Shin, Su Ryon Tullius, Stefan G. Bromberg, Jonathan S. Sage, Peter T. Abdi, Reza Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node |
title | Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node |
title_full | Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node |
title_fullStr | Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node |
title_full_unstemmed | Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node |
title_short | Characterization of Leptin Receptor(+) Stromal Cells in Lymph Node |
title_sort | characterization of leptin receptor(+) stromal cells in lymph node |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8801441/ https://www.ncbi.nlm.nih.gov/pubmed/35111151 http://dx.doi.org/10.3389/fimmu.2021.730438 |
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