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Review
. 2023 Nov 14;2(1):kyad022.
doi: 10.1093/discim/kyad022. eCollection 2023.

Eosinophils in obesity and obesity-associated disorders

Affiliations
Review

Eosinophils in obesity and obesity-associated disorders

Yanan Hu et al. Discov Immunol. .

Abstract

Despite the rising prevalence and costs for the society, obesity etiology, and its precise cellular and molecular mechanisms are still insufficiently understood. The excessive accumulation of fat by adipocytes plays a key role in obesity progression and has many repercussions on total body physiology. In recent years the immune system as a gatekeeper of adipose tissue homeostasis has been evidenced and has become a focal point of research. Herein we focus on eosinophils, an important component of type 2 immunity, assuming fundamental, yet ill-defined, roles in the genesis, and progression of obesity and related metabolic disorders. We summarize eosinophilopoiesis and eosinophils recruitment into adipose tissue and discuss how the adipose tissue environments shape their function and vice versa. Finally, we also detail how obesity transforms the local eosinophil niche. Understanding eosinophil crosstalk with the diverse cell types within the adipose tissue environment will allow us to framework the therapeutic potential of eosinophils in obesity.

Keywords: adipose tissue; eosinophil; immune metabolism; obesity.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Graphical Abstract
Graphical Abstract
Figure 1:
Figure 1:
adipose tissue eosinophils differentiation and recruitment. Eosinophils develop in the bone marrow (BM), from granulocyte/macrophage progenitors (GMP), to mature eosinophils passing by eosinophil-lineage-committed progenitors (EoP) stage. This transition implies the expression of various transcriptional factors such as CEBPs GATA1 and XBP1 and under the control of cytokines such as IL5, IL33, and GM-CSF. Eosinophils exit the BM into peripheral blood as mature cells expressing Siglec-F, CCR3, and ST2. Recruitment of eosinophils in adipose tissue (AT) depends on CCL11 secretion by AT niche. The extravasation of eosinophils depends on their interaction with endothelial cells via molecules such as ICAM1, VICAM1 expressed by endothelium and CD162, α4β1, αLβ2, αMβ2 on eosinophils. In the AT, AT-derived factors promote AT eosinophils (ATE) reprograming and subsequent ATE-specific function.
Figure 2:
Figure 2:
ATE niche. Different AT cell components will provide distinct signals that will dictate ATE specific functions. Inversely ATE will provide signals controlling the AT environment.

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