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Published in: Clinical Reviews in Allergy & Immunology 3/2020

Open Access 01-06-2020 | Obesity

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

Authors: Daniel Elieh Ali Komi, Farzaneh Shafaghat, Mark Christian

Published in: Clinical Reviews in Allergy & Immunology | Issue 3/2020

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Abstract

Excessive fatty acids and glucose uptake support the infiltration of adipose tissue (AT) by a variety of immune cells including neutrophils, pro-inflammatory M1 macrophages, and mast cells (MCs). These cells promote inflammation by releasing pro-inflammatory mediators. The involvement of MCs in AT biology is supported by their accumulation in the AT of obese individuals along with significantly higher serum levels of MC-derived tryptase. AT-resident MCs under the influence of locally derived adipokines such as leptin become activated and release pro-inflammatory cytokines including TNFα that worsens the inflammatory state. MCs support angiogenesis in AT by releasing chymase and inducing preadipocyte differentiation and also the proliferation of adipocytes through 15-deoxy-delta PGJ2/PPARγ interaction. Additionally, they contribute to the remodeling of the AT extracellular matrix (ECM) and play a role in the recruitment and activation of leukocytes. MC degranulation has been linked to brown adipocyte activation, and evidence indicates an important link between MCs and the appearance of BRITE/beige adipocytes in white AT. Cell crosstalk between MCs and AT-resident cells, mainly adipocytes and immune cells, shows that these cells play a critical role in the regulation of AT homeostasis and inflammation.
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Metadata
Title
Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions
Authors
Daniel Elieh Ali Komi
Farzaneh Shafaghat
Mark Christian
Publication date
01-06-2020
Publisher
Springer US
Keywords
Obesity
Obesity
Published in
Clinical Reviews in Allergy & Immunology / Issue 3/2020
Print ISSN: 1080-0549
Electronic ISSN: 1559-0267
DOI
https://doi.org/10.1007/s12016-020-08785-7

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