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LKB1 regulates adipose tissue ILC2 function through regulating mitochonrial

ABSTRACT: Our study represents LKB1 defects lead to the loss and dysfunction of adipose tissue ILC2s.And we found that LKB1 regulate ILC2s homeostasis and cytokines function in a cell-intrinsic manner.In high-diet-fed mice,LKB1 in ILC2s protects against metabolic disturbances and fat fibrosis.LKB1 deficient in ILC2 impaired the oxidative phosphorylation and led to mitochondria loss though more mitophagy.

ORGANISM(S): Mus musculus

PROVIDER: GSE225097 | GEO | 2025/09/17

REPOSITORIES: GEO

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LKB1 regulates adipose tissue ILC2 function through regulating mitochonrial

Project description:Our study represents LKB1 defects lead to the loss and dysfunction of adipose tissue ILC2s.And we found that LKB1 regulate ILC2s homeostasis and cytokines function in a cell-intrinsic manner.In high-diet-fed mice,LKB1 in ILC2s protects against metabolic disturbances and fat fibrosis.LKB1 deficient in ILC2 impaired the oxidative phosphorylation and led to mitochondria loss though more mitophagy.

2025-09-17 | GSE196196 | GEO

LKB1 prevents ILC2 exhaustion and lung cancer metastasis

Project description:Group 2 innate lymphoid cells (ILC2s) mediate type 2 immune responses involved in anti-helminth immunity, allergic inflammation, and metabolic homeostasis. Recently, they have emerged as key players in regulating tumor immunity. The tumor suppressor liver kinase B1 (LKB1) inactivating mutations is associated with a variety of human cancers, but the role of LKB1 in ILC2 function and ILC2-mediated tumor immunity remains unknown. Here, we show that LKB1 is required for mature ILC2 survival. Ablation of LKB1 in ILC2s results in impaired proliferation and a marked decrease in type 2 cytokine production upon activation, accompanied with the expression of exhaustion signature genes and reduced cellular metabolism, which promote the development of lung melanoma metastasis. In addition, LKB1 deficiency leads to a marked increase of programmed cell death protein-1 (PD-1) expression in ILC2s through activation of nuclear factor of activated T cells (NFAT) pathway. Blockade of PD-1 can restore type 2 cytokine production in LKB1-deficient ILC2 and reverse its exhaustion state, leading to enhanced antitumor immune responses in vivo. Together, our results reveal that LKB1 retrains ILC2 exhaustion state to maintain immune homeostasis and their antitumor immunity.

2024-05-21 | GSE209588 | GEO

LKB1 regulates adipose tissue ILC2 function through regulating mitochonrial

Project description:LKB1 regulates adipose tissue ILC2 function through regulating mitochonrial

| PRJNA803884 | ENA

LKB1 regulates adipose tissue ILC2 function through regulating mitochonrial

Project description:LKB1 regulates adipose tissue ILC2 function through regulating mitochonrial

| PRJNA933912 | ENA

Human ILC2 cells stimulated with IL-25, IL-33, or TSLP

Project description:ILC2 cells are a newly described cell type whose biology and contribution to disease are poorly understood. ILC2 cells are activated by allergens, viral infection, and/or epithelial damage via IL-33 and IL-25. ILC2 cells require IL-2, IL-7, IL-25 and IL-33 for their survival and expansion. In mice, ILC2s produce multiple mediators primarily associated with type 2 inflammation (IL-13, IL-5, IL-4, IL-6, IL-9, IL-10, GM-CSF, amphiregulin). ILC2 cells may contribute to the pathology of asthma through multiple mediators that include IL-13-independent pathways. Our goal is to compare transcriptional profiles of IL-33- or IL-25-activated ILC2 cells from blood to characterize these cells and to identify marker(s) that can be utilized to detect them in human tissue. ILC2 cells (Lineage negative, CRTH2+, CD161+, CD127+) were purified from human blood of 5 different donors by flow cytometry. The ILC2 yield ranged from 20,000 to 165,000 cells per donor (0.001-0.008% WBC). Purified ILC2s were expanded in vitro in the presence of IL-2, IL-7, IL-33 and IL-25 (each at 50 ng/ml) for 7-10 days. Expanded cells maintained the ILC2 phenotype (Lineage negative, CRTH2+, CD161+, CD127+). The cells were rested for 2 days in the presence of 1 ng/ml IL-2 and IL-7 and then treated in the presence of 1 ng/ml IL-2 and IL-7 with either media control, IL-25 (50 ng/ml), IL-33 (50 ng/ml), and/or TSLP (50 ng/ml) in combination, for 6 or 24 hours. Whole RNA was isolated via the RNeasy kit (Qiagen). Stratagene Universal Human Reference RNA was used as the reference.

2013-12-31 | E-GEOD-45458 | biostudies-arrayexpress

mTORC1 controls ILC2 activation and allergic lung inflammation through NMUR1-mediated neuronal regulation

Project description:Group 2 innate lymphoid cells (ILC2s) play critical roles in allergic lung inflammation through initiating and amplifying type 2 immune responses. However, the molecular mechanisms underlying pathogenic ILC2 activation remain largely unknown. Here, we show that lung ILC2s exhibit increased mTORC1 activation in allergic asthma. Genetic ablation of RAPTOR, an adaptor protein of the mTORC1 complex, results in reduced IL-5 and IL-13 production in ILC2s and protects mice from allergic inflammation. Pharmacological inhibition of mTORC1 by rapamycin also suppresses ILC2 pathogenic activation and ameliorates allergic lung inflammation. Mechanistically, mTORC1 signaling promotes ILC2 activation through metabolic regulation of epigenetics to maintain neurointerin U receptor 1 (NMUR1) expression, which mediates neural-ILC2 interaction via the NMU-NMUR1 axis. These findings identify mTORC1 as a novel regulator to control the neural-ILC2 interaction and highlight mTORC1 as a potential therapeutic target for allergic asthma.

2025-10-30 | GSE272521 | GEO

LKB1 prevents ILC2 exhaustion and lung cancer metastasis

Project description:LKB1 prevents ILC2 exhaustion and lung cancer metastasis

| PRJNA861294 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of DR-3 agonist on sorted mouse VAT ILC2 Transcriptomes

Project description:Disturbances in glucose homeostasis and low-grade chronic inflammation culminate into metabolic syndrome that increase the risk for the development of type 2 diabetes mellitus (T2DM). The recently discovered type 2 innate lymphoid cells (ILC2s) are capable of secreting copious amounts of type 2 cytokines to modulate metabolic homeostasis in adipose tissue. In this study, we have established that expression of Death Receptor 3 (DR3), a member of the TNF superfamily, on visceral adipose tissue (VAT)-derived murine and peripheral blood human ILC2s is inducible by IL-33. We demonstrate that DR3 engages the canonical and/or non-canonical NF-B pathways, and thus stimulates naïve and co-stimulates IL-33-activated ILC2s. Importantly, DR3 engagement on ILC2s significantly ameliorates glucose tolerance, protects against insulin-resistance onset and remarkably reverses already established insulin-resistance. Taken together, these results convey the potent role of DR3 as an ILC2 regulator and introduce DR3 agonistic treatment as a novel therapeutic avenue for treating T2DM.

2020-07-22 | GSE154823 | GEO

mTORC1 controls ILC2 activation and allergic lung inflammation through NMUR1-mediated neuronal regulation [WT-KO ILC2s RNA-seq]

2025-10-30 | GSE272716 | GEO

Iron controls the development of airway hyperreactivity by regulating ILC2 metabolism and effector function

Project description:Group 2 innate lymphoid cells (ILC2s) rapidly induce a type 2 inflammation in the lungs in response to allergens. Here, we focused on the role of iron – a critical nutritional trace element – on ILC2 function and asthma pathogenesis. In the lungs, transferrin receptor 1 (TfR1) is rapidly upregulated and functional during ILC2 activation, while blocking transferrin uptake reduces ILC2 expansion and activation. Iron deprivation reprograms ILC2 metabolism, inducing a HIF-1a-driven upregulation of glycolysis and inhibition of oxidative mitochondrial activity. Consequently, in vivo iron chelation or induction of hypoferremia notably reduces the development of airway hyperreactivity in experimental models of ILC2-driven allergic asthma. Human circulating ILC2s rapidly induce TfR1 during activation, while iron deprivation reduces effector functions. Finally, we found a negative relation between circulating ILC2 TfR1 expression and airway function in cohorts of patients with asthma. Collectively, our studies define cellular iron as a critical regulator of ILC2 function.

2024-05-21 | GSE262210 | GEO

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