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LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE128475 | GEO | 2019/04/16

REPOSITORIES: GEO

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LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity.

Project description:Dendritic cells (DCs) play a pivotal role in priming adaptive immunity. However, the involvement of DCs in controlling excessive and deleterious T cell responses remains poorly defined. Moreover, the metabolic dependence and regulation of DC function are unclear. Here we show that LKB1 signaling in DCs functions as a brake to restrain excessive tumor-promoting regulatory T cell (Treg) and Th17 cell responses, thereby promoting protective anti-tumor immunity and maintaining proper immune homeostasis. LKB1 deficiency results in dysregulated metabolism and mTOR activation of DCs. Loss of LKB1 also leads to aberrant DC maturation and production of cytokines and immunoregulatory molecules. Blocking mTOR signaling in LKB1-deficient DCs partially rectifies the abnormal phenotypes of DC activation and Treg expansion, whereas uncontrolled Th17 responses depend upon IL-6-STAT3 signaling. By coordinating metabolic and immune quiescence of DCs, LKB1 acts as a crucial signaling hub in DCs to enforce protective anti-tumor immunity and normal immune homeostasis.

| S-EPMC6796952 | biostudies-literature

LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity [HT_MG-430_PM]

Project description:Loss of LKB1 leads to aberrant DC maturation and production of cytokines and immunoregulatory molecules. DCs (n = 7 per genotype) were isolated from the spleen, and CD25+CD4+ Tregs (n = 4 for WT, n = 3 for LKB1ΔDC mice) were isolated from the spleen and peripheral lymph nodes of WT and LKB1ΔDC mice.

2019-04-16 | GSE128474 | GEO

LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity [MoGene-2_0-st]

2019-04-16 | GSE128473 | GEO

LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity

Project description:LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity

| PRJNA527815 | ENA

LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity [HT_MG-430_PM]

Project description:LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity [HT_MG-430_PM]

| PRJNA527819 | ENA

LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity [MoGene-2_0-st]

Project description:LKB1 orchestrates dendritic cell metabolic quiescence and anti-tumor immunity [MoGene-2_0-st]

| PRJNA527817 | ENA

PROX1 Orchestrates Tumor Metabolic Plasticity by Integrating LKB1-AMPK Signaling with BCAA Catabolism

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-27 | GSE214194 | GEO

KDM5A epigenetically orchestrates MHC-I associated anti-tumor immunity of immunotherapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-03-31 | GSE256057 | GEO

RNA m6A-Ythdf1 in dendritic cells triggers anti-tumor immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-12-29 | GSE115106 | GEO

Lkb1 regulates quiescence and metabolic homeostasis of haematopoietic stem cells.

Project description:The capacity to fine-tune cellular bioenergetics with the demands of stem-cell maintenance and regeneration is central to normal development and ageing, and to organismal survival during periods of acute stress. How energy metabolism and stem-cell homeostatic processes are coordinated is not well understood. Lkb1 acts as an evolutionarily conserved regulator of cellular energy metabolism in eukaryotic cells and functions as the major upstream kinase to phosphorylate AMP-activated protein kinase (AMPK) and 12 other AMPK-related kinases. Whether Lkb1 regulates stem-cell maintenance remains unknown. Here we show that Lkb1 has an essential role in haematopoietic stem cell (HSC) homeostasis. We demonstrate that ablation of Lkb1 in adult mice results in severe pancytopenia and subsequent lethality. Loss of Lkb1 leads to impaired survival and escape from quiescence of HSCs, resulting in exhaustion of the HSC pool and a marked reduction of HSC repopulating potential in vivo. Lkb1 deletion has an impact on cell proliferation in HSCs, but not on more committed compartments, pointing to context-specific functions for Lkb1 in haematopoiesis. The adverse impact of Lkb1 deletion on haematopoiesis was predominantly cell-autonomous and mTOR complex 1 (mTORC1)-independent, and involves multiple mechanisms converging on mitochondrial apoptosis and possibly downregulation of PGC-1 coactivators and their transcriptional network, which have critical roles in mitochondrial biogenesis and function. Thus, Lkb1 serves as an essential regulator of HSCs and haematopoiesis, and more generally, points to the critical importance of coupling energy metabolism and stem-cell homeostasis.

| S-EPMC3058342 | biostudies-literature

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