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CD36 Triggers a non-classical lipid metabolic Program promoting Immune Escape and Resistance to HMA therapy in AML

ABSTRACT: CD36 Triggers a non-classical lipid metabolic Program promoting Immune Escape and Resistance to HMA therapy in AML

PROVIDER: PRJNA935375 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23489700_1.fastq.gz	Fastqsanger.gz
	SRR23489700_2.fastq.gz	Fastqsanger.gz
	SRR23489701_1.fastq.gz	Fastqsanger.gz
	SRR23489701_2.fastq.gz	Fastqsanger.gz
	SRR23489702_1.fastq.gz	Fastqsanger.gz

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CD36 Triggers a non-classical lipid metabolic Program promoting Immune Escape and Resistance to HMA therapy in AML

Project description:To investigate the effect of decitabine on CD36/NFkB/TLR signaling pathway in MV4-11 cells, and to explore the CD36-dependent signaling pathway regulated by decitabine. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells at two different treatment.

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Project description:Monocytes can be classified into four different subsets: classic, intermediate and SLAN- and SLAN+ non-classical monocytes. SLAN+ monocytes are significantly reduced in MM patients compare to the frequency found in healthy adults (HA). Thus, we sought to analyze the transcriptome of SLAN- and SLAN+ cells to unveil the differences among both populations We used microarrays to detail the global programme of gene expression underlying the differences among both cell subsets We developed a 12-color combination of mAbs to evaluate the contribution of each individual marker for identifying and subsetting BM TAMs in patients with MM (N = 5): CD36-UV405, CD16-UV525, CD163-BV450, CD45-BV525, CD206-BV610, CD86-BV660, CD62L-BV763, cyCD68-FITC, SLAN-PE, HLADR-PerCPCy5.5, CD300e-APC, CD14-APCH7. This panel allowed us to identify the aforementioned four monocyte subsets. Intermediate and non-classical monocytes from healthy donors were FACS sorted based on the 7-color mAb combination - HLADR-PacB, CD45-OC515, CD36-FITC, SLAN-PE, CD16-PECy7, CD300e-APC, CD14APCH7 -

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Gene expression differences between LPS, anti-CD36 Abs, or LPS plus anti-CD36 Abs treated RAW264.7 cells.

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Single cell RNA sequencing of peritoneal cells from macrophage-Cd36-/- and macrophage-Cd36 fl/fl mice at the resolution phase of sterile inflammation.

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Hypoxia-inducible factor 2α attenuates renal ischemia-reperfusion injury by suppressing CD36-mediated lipid accumulation in dendritic cells

Project description:Hypoxia is a hallmark of renal ischemia reperfusion injury (IRI) and serves as an essential regulator of innate immune responses during this process, although the mechanisms of this regulation remain unclear. Here, we show that dendritic cell (DC)-specific genetic ablation of hypoxia-inducible factor (HIF) 2α, a transcription factor induced by oxygen shortage, leads to hyperactivation of natural killer T cells (NKTs), ultimately exacerbating renal IRI in mice. HIF-2α deficiency in DCs triggers IFN-γ and IL-4 production in NKTs, along with upregulation of type I interferon (IFN) and chemokine responses critical for NKT activation. Mechanistically, loss of HIF-2α in DCs promotes their expression of CD36, a scavenger receptor for lipid uptake, resulting in increased lipid accumulation. Furthermore, HIF-2α binds directly to a reverse hypoxia-responsive element (rHRE) in the CD36 promoter, supporting its transcriptional regulation of CD36. Importantly, CD36 blockade by sulfo-N-succinimidyl oleate (SSO), reduces NKT activation and abolishes the exacerbation of renal IRI in mice with DC-specific HIF-2α knockout. Taken together, our study reveals a previously unrecognized role of a HIF-2α-CD36 regulatory axis in rewiring DC lipid metabolism under IRI-associated hypoxia, and suggests a potential therapeutic target to resolve long-standing obstacles in clinical treatment of this severe complication.

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