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B Cell-Mediated Crosstalk With Macro...

Carey, Anna,

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B Cell-Mediated Crosstalk With Macrophages in Adipose Tissue: Key Modulators of Inflammation and Metabolism During Aging /

Record Type:	Electronic resources : Monograph/item
Title/Author:	B Cell-Mediated Crosstalk With Macrophages in Adipose Tissue: Key Modulators of Inflammation and Metabolism During Aging // Anna Carey.
Author:	Carey, Anna,
Description:	1 electronic resource (169 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 86-07, Section: A.
Contained By:	Dissertations Abstracts International86-07A.
Subject:	Aging. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31767270
ISBN:	9798302185259

B Cell-Mediated Crosstalk With Macrophages in Adipose Tissue: Key Modulators of Inflammation and Metabolism During Aging /
Carey, Anna,

B Cell-Mediated Crosstalk With Macrophages in Adipose Tissue: Key Modulators of Inflammation and Metabolism During Aging /Anna Carey. - 1 electronic resource (169 pages)

Source: Dissertations Abstracts International, Volume: 86-07, Section: A.

Visceral white adipose tissue (VATa ) is a tissue to show early indications of aging including the upregulation of transcriptional pathways associated with inflammation and immune activation, shifting of the immune landscape, and metabolic dysfunction. B cells accumulate in VAT in response to inflammatory signals including IL-1β and were previously shown to promote metabolic dysfunction. The goal of this dissertation is to dissect mechanisms by which adipose B cells drive age-associated dysfunction and regulate their microenvironment in the VAT. We identified that non-canonical lipolysis induced by sepsis and endotoxemia, a metabolic process required for the regulation of inflammation, is impaired in the VAT of old mice. We found using a mouse model of life-long B cell deficiency that B cells drive impaired noncanonical lipolysis and pro-inflammatory macrophage phenotypes. We hypothesized that IL-1β may signal B cells to drive these phenotypes. To test this, we utilized an aging model of B cell selective IL1R1 knockout (BKO) and single cell RNA sequencing to investigate the contribution of this signaling pathway to aged VAT immune cell inflammatory profiles. We identified that IL-1β signaling on B cells results in differentially affected immune cell populations including the immunosuppression of MHCIIhi inflammatory macrophages that increase during aging. Finally, we describe how B cell-macrophage dependent production of TGFβ likely drives the suppression of noncanonical lipolysis in the VAT of old mice. Overall, the data presented in this dissertation outline how adipose B cells and macrophage crosstalk regulates VAT aging to promote metabolic dysfunction and inflammation but also has nuanced immunosuppressive roles in response to specific signals including IL-1β. We propose that the B cell-macrophage signaling axis in the VAT is an appealing therapeutic target to improve metabolism, ameliorate age-associated inflammation, and reduce mortality during infections in elderly populations.

English

ISBN: 9798302185259Subjects--Topical Terms:

543123
Aging.
Subjects--Index Terms:

Adipose tissue

B Cell-Mediated Crosstalk With Macrophages in Adipose Tissue: Key Modulators of Inflammation and Metabolism During Aging /
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520 $a Visceral white adipose tissue (VATa ) is a tissue to show early indications of aging including the upregulation of transcriptional pathways associated with inflammation and immune activation, shifting of the immune landscape, and metabolic dysfunction. B cells accumulate in VAT in response to inflammatory signals including IL-1β and were previously shown to promote metabolic dysfunction. The goal of this dissertation is to dissect mechanisms by which adipose B cells drive age-associated dysfunction and regulate their microenvironment in the VAT. We identified that non-canonical lipolysis induced by sepsis and endotoxemia, a metabolic process required for the regulation of inflammation, is impaired in the VAT of old mice. We found using a mouse model of life-long B cell deficiency that B cells drive impaired noncanonical lipolysis and pro-inflammatory macrophage phenotypes. We hypothesized that IL-1β may signal B cells to drive these phenotypes. To test this, we utilized an aging model of B cell selective IL1R1 knockout (BKO) and single cell RNA sequencing to investigate the contribution of this signaling pathway to aged VAT immune cell inflammatory profiles. We identified that IL-1β signaling on B cells results in differentially affected immune cell populations including the immunosuppression of MHCIIhi inflammatory macrophages that increase during aging. Finally, we describe how B cell-macrophage dependent production of TGFβ likely drives the suppression of noncanonical lipolysis in the VAT of old mice. Overall, the data presented in this dissertation outline how adipose B cells and macrophage crosstalk regulates VAT aging to promote metabolic dysfunction and inflammation but also has nuanced immunosuppressive roles in response to specific signals including IL-1β. We propose that the B cell-macrophage signaling axis in the VAT is an appealing therapeutic target to improve metabolism, ameliorate age-associated inflammation, and reduce mortality during infections in elderly populations.
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