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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
The systemic characteristics of iNature fat-regulated T (Treg) cell subsets and their phenotypes are still uncommon
.
On August 24, 2021, Li Bin, Tong Xuemei of Shanghai Jiaotong University and Wang Gang of Fudan University jointly published a research paper titled "Insulin signaling establishes a developmental trajectory of adipose regulatory T cells" in Nature Immunology.
The study uses single-cell ATAC.
Sequencing and pairing single-cell RNA and T cell receptor (TCR) sequencing to map mouse fat Treg cells, identified CD73hiST2lo and CD73loST2hi subpopulations with different clonal expansion patterns
.
The analysis of TCR shared data implies a state transition between CD73hiST2lo and CD73loST2hi subsets
.
In terms of mechanism, the study found that insulin signaling occurs through the HIF-1α-Med23-PPAR-γ axis to drive the conversion of CD73hiST2lo into CD73loST2hi adipose Treg cell subsets
.
Treg cells lacking insulin receptor, HIF-1α or Med23 reduce the expression of PPAR-γ, which in turn promotes the accumulation of CD73hiST2lo fat Treg cells and the production of physiological adenosine, thereby activating the biogenesis of beige fat
.
Therefore, this study revealed the developmental trajectory of adipose Treg cells and their dependence on insulin signaling
.
The results of this study have important implications for understanding the dynamics of adipose Treg cell subpopulations in the elderly and obese environments
.
Immune cells with regulating phenotype have important auxiliary functions and can prevent systemic metabolic disorders
.
Treg cells from adipose tissue express a large number of transcription factors PPAR-γ, which inhibit the activity of effector T (Teff) cells and other immune cell types under physiological conditions, maintain insulin sensitivity, and control systemic metabolic homeostasis
.
It is worth noting that adipose Treg cells express a unique TCR library, and the specificity of TCR may drive PPAR-γ expression through the transcriptional regulators IRF4 and BATF
.
Other reports further indicate that the accumulation of adipose Treg cells requires major histocompatibility complex class II molecules, interleukin (IL)-33, and antigens for the presentation of sex hormones and insulin signals
.
In addition, the transcription factor BLIMP1 activates the expression of IL-33 receptor ST2 (Il1rl1), thus promoting IL-33-mediated adipose Treg cell expansion
.
These studies mainly found the unique molecular characteristics of adipose Treg cells at the entire population level, but the systemic characteristics and corresponding physiological effects of its subpopulations are still uncommon
.
Although previous insights revealed the insulin sensitization of adipose Treg cells, their role and predictive potential under different physiological conditions are still controversial
.
In obese fat, adipose Treg cells suppress overactive immune responses and help maintain insulin sensitivity
.
However, in aging fat, the researchers reported an opposite effect, that the increase in fat Treg cell accumulation failed to prevent age-related insulin resistance
.
Depletion of PPAR-γ+ or IL-33 receptor ST2hi adipose Treg cells significantly improved insulin sensitivity in aged mice
.
It is conceivable that adipose Treg cells diversify into a series of states and exert different physiological effects in the body
.
For these reasons, the systematic characterization of adipose Treg cell subpopulations with known TCR and transcriptome information is valuable for coordinating the aforementioned differential observations in the elderly and obese environments
.
In addition, the molecular programs that drive state transitions between subpopulations of adipose Treg cells are not well understood
.
To solve this problem, the integration of single-cell assays of transposase-accessible chromatin using sequencing (scATAC sequencing) and single-cell RNA sequencing (scRNA-seq) data may help reveal closely related staining of adipose Treg cell subpopulations Qualitative differences and over-expressed transcription factor motifs
.
To solve this problem, the study performed scATAC-seq and paired scRNA-seq and TCR sequencing (TCR-seq) here to reveal the chromatin landscape, regulatory modules, clonal structure, and phenotype of adipose Treg cell subsets
.
Although several previous studies have used scRNA-seq or a large amount of ATAC-seq data to describe the internal transcription program of tissue Treg cells, this study contains comprehensive single-cell data with paired TCR information, which facilitates more in-depth analysis of fat Treg The molecular mechanism of state transition between cell subpopulations
.
In order to verify these findings, the study used conditional knockout mouse models and in vitro cell assays to reveal how insulin signaling occurs through the HIF-1α–Med23–PPAR-γ axis to drive the conversion of CD73hiST2lo into CD73loST2hi adipose Treg cell subsets, and revealed The unique physiological effects of CD73hiST2lo adipose Treg cell subsets on beige fat biogenesis and insulin sensitivity
.
In addition, the study proposes a new mechanism model that reveals the dynamics of adipose Treg cell subsets in the elderly and obese environments
.
The findings of this study may have implications for the development of new therapies for the treatment of age-related or diet-induced insulin resistance
.
Reference message: https://
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
The systemic characteristics of iNature fat-regulated T (Treg) cell subsets and their phenotypes are still uncommon
.
On August 24, 2021, Li Bin, Tong Xuemei of Shanghai Jiaotong University and Wang Gang of Fudan University jointly published a research paper titled "Insulin signaling establishes a developmental trajectory of adipose regulatory T cells" in Nature Immunology.
The study uses single-cell ATAC.
Sequencing and pairing single-cell RNA and T cell receptor (TCR) sequencing to map mouse fat Treg cells, identified CD73hiST2lo and CD73loST2hi subpopulations with different clonal expansion patterns
.
The analysis of TCR shared data implies a state transition between CD73hiST2lo and CD73loST2hi subsets
.
In terms of mechanism, the study found that insulin signaling occurs through the HIF-1α-Med23-PPAR-γ axis to drive the conversion of CD73hiST2lo into CD73loST2hi adipose Treg cell subsets
.
Treg cells lacking insulin receptor, HIF-1α or Med23 reduce the expression of PPAR-γ, which in turn promotes the accumulation of CD73hiST2lo fat Treg cells and the production of physiological adenosine, thereby activating the biogenesis of beige fat
.
Therefore, this study revealed the developmental trajectory of adipose Treg cells and their dependence on insulin signaling
.
The results of this study have important implications for understanding the dynamics of adipose Treg cell subpopulations in the elderly and obese environments
.
Immune cells with regulating phenotype have important auxiliary functions and can prevent systemic metabolic disorders
.
Treg cells from adipose tissue express a large number of transcription factors PPAR-γ, which inhibit the activity of effector T (Teff) cells and other immune cell types under physiological conditions, maintain insulin sensitivity, and control systemic metabolic homeostasis
.
It is worth noting that adipose Treg cells express a unique TCR library, and the specificity of TCR may drive PPAR-γ expression through the transcriptional regulators IRF4 and BATF
.
Other reports further indicate that the accumulation of adipose Treg cells requires major histocompatibility complex class II molecules, interleukin (IL)-33, and antigens for the presentation of sex hormones and insulin signals
.
In addition, the transcription factor BLIMP1 activates the expression of IL-33 receptor ST2 (Il1rl1), thus promoting IL-33-mediated adipose Treg cell expansion
.
These studies mainly found the unique molecular characteristics of adipose Treg cells at the entire population level, but the systemic characteristics and corresponding physiological effects of its subpopulations are still uncommon
.
Although previous insights revealed the insulin sensitization of adipose Treg cells, their role and predictive potential under different physiological conditions are still controversial
.
In obese fat, adipose Treg cells suppress overactive immune responses and help maintain insulin sensitivity
.
However, in aging fat, the researchers reported an opposite effect, that the increase in fat Treg cell accumulation failed to prevent age-related insulin resistance
.
Depletion of PPAR-γ+ or IL-33 receptor ST2hi adipose Treg cells significantly improved insulin sensitivity in aged mice
.
It is conceivable that adipose Treg cells diversify into a series of states and exert different physiological effects in the body
.
For these reasons, the systematic characterization of adipose Treg cell subpopulations with known TCR and transcriptome information is valuable for coordinating the aforementioned differential observations in the elderly and obese environments
.
In addition, the molecular programs that drive state transitions between subpopulations of adipose Treg cells are not well understood
.
To solve this problem, the integration of single-cell assays of transposase-accessible chromatin using sequencing (scATAC sequencing) and single-cell RNA sequencing (scRNA-seq) data may help reveal closely related staining of adipose Treg cell subpopulations Qualitative differences and over-expressed transcription factor motifs
.
To solve this problem, the study performed scATAC-seq and paired scRNA-seq and TCR sequencing (TCR-seq) here to reveal the chromatin landscape, regulatory modules, clonal structure, and phenotype of adipose Treg cell subsets
.
Although several previous studies have used scRNA-seq or a large amount of ATAC-seq data to describe the internal transcription program of tissue Treg cells, this study contains comprehensive single-cell data with paired TCR information, which facilitates more in-depth analysis of fat Treg The molecular mechanism of state transition between cell subpopulations
.
In order to verify these findings, the study used conditional knockout mouse models and in vitro cell assays to reveal how insulin signaling occurs through the HIF-1α–Med23–PPAR-γ axis to drive the conversion of CD73hiST2lo into CD73loST2hi adipose Treg cell subsets, and revealed The unique physiological effects of CD73hiST2lo adipose Treg cell subsets on beige fat biogenesis and insulin sensitivity
.
In addition, the study proposes a new mechanism model that reveals the dynamics of adipose Treg cell subsets in the elderly and obese environments
.
The findings of this study may have implications for the development of new therapies for the treatment of age-related or diet-induced insulin resistance
.
Reference message: https://
