Resident and migratory adipose immune cells control systemic metabolism and thermogenesis

Glucose is a vital source of energy for all mammals.The balance between glucose uptake,metabolism and storage determines the energy status of an individual,and perturbations in this balance can lead to metabolic diseases.The maintenance of organismal glucose metabolism is a complex process that involves multiple tissues,including adipose tissue,which is an endocrine and energy storage organ that is critical for the regulation of systemic metabolism.Adipose tissue consists of an array of different cell types,including specialized adipocytes and stromal and endothelial cells.In addition,adipose tissue harbors a wide range of immune cells that play vital roles in adipose tissue homeostasis and function.These cells contribute to the regulation of systemic metabolism by modulating the inflammatory tone of adipose tissue,which is directly linked to insulin sensitivity and signaling.Furthermore,these cells affect the control of thermogenesis.While lean adipose tissue is rich in type 2 and anti-inflammatory cytokines such as IL-10,obesity tips the balance in favor of a proinflammatory milieu,leading to the development of insulin resistance and the dysregulation of systemic metabolism.Notably,anti-inflammatory immune cells,including regulatory T cells and innate lymphocytes,protect against insulin resistance and have the characteristics of tissue-resident cells,while proinflammatory immune cells are recruited from the circulation to obese adipose tissue.Here,we review the key findings that have shaped our understanding of how immune cells regulate adipose tissue homeostasis to control organismal metabolism.

Correction: Resident and migratory adipose immune cells control systemic metabolism and thermogenesis

Correction to:Cellular&Molecular Immunology https://doi.org/10.1038/s41423-021-00804-7,published online 26 November 2021 The article Resident and migratory adipose immune cells control systemic metabolism and thermogenesis,written by Kevin Man,Axel Kallies and Ajithkumar Vasanthakumar was originally published electronically on the publisher’s internet portal on 24.11.2021 without open access.

CCR2 enhances CD25 expression by FoxP3^(+) regulatory T cells and regulates their abundance independently of chemotaxis and CCR2^(+) myeloid cells

A wide array of chemokine receptors,including CCR2,are known to control Treg migration.Here,we report that CCR2 regulates Tregs beyond chemotaxis.We found that CCR2 deficiency reduced CD25 expression by FoxP3^(+) Treg cells.Such a change was also consistently present in irradiation chimeras reconstituted with mixed bone marrow from wild-type(WT)and CCR2−/−strains.Thus,CCR2 deficiency resulted in profound loss of CD25 ^(hi) FoxP3^(+) Tregs in secondary lymphoid organs as well as in peripheral tissues.CCR2−/−Treg cells were also functionally inferior to WT cells.Interestingly,these changes to Treg cells did not depend on CCR2+monocytes/moDCs(the cells where CCR2 receptors are most abundant).Rather,we demonstrated that CCR2 was required for TLR-stimulated,but not TCR-or IL-2-stimulated,CD25 upregulation on Treg cells.Thus,we propose that CCR2 signaling can increase the fitness of FoxP3^(+) Treg cells and provide negative feedback to counter the proinflammatory effects of CCR2 on myeloid cells.