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PLT012, a humanized CD36-blocking antibody, is effective for unleashing anti-tumor immunity against liver cancer and liver metastasis

ABSTRACT: PLT012, a humanized CD36-blocking antibody, is effective for unleashing anti-tumor immunity against liver cancer and liver metastasis

PROVIDER: PRJNA1236262 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32698976_1.fastq.gz	Fastqsanger.gz
	SRR32698976_2.fastq.gz	Fastqsanger.gz
	SRR32698977_1.fastq.gz	Fastqsanger.gz
	SRR32698977_2.fastq.gz	Fastqsanger.gz

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PLT012, a humanized CD36-blocking antibody, is effective for unleashing anti-tumor immunity against liver cancer and liver metastasis

Project description:Tumor cells develop various strategies to evade immune surveillance, one of which is the modulation of the metabolic state of the tumor microenvironment (TME). In response to metabolic stress in the TME, several tumor-infiltrating immune subsets upregulate CD36 to take up lipids. This leads to impaired anti-tumor immunity, as intratumoral regulatory T cells (Tregs) exhibit increased survival and suppressive activity, while CD8+ T cells become more susceptible to ferroptosis and exhaustion. Here, we develop a humanized anti-CD36 IgG4 antibody, PLT012, against the lipid-binding domain of CD36 with excellent safety and favorable pharmacokinetic features in mice and cynomolgus monkey. PLT012 alone or in combination with PD-L1 blockade or standard-of-care immunotherapy results in robust anti-tumor immunity in both immunotherapy-sensitive and -resistant hepatocellular carcinomas (HCCs). Notably, PLT012 also reprograms immune landscape of human HCC ex vivo. Our findings provide proof-of-concept evidence that PLT012 effectively reprograms anti-tumor immunity in HCC, positioning it as a first-in-class immunotherapy targeting CD36.

2025-04-11 | GSE291964 | GEO

PLT012, a Humanized CD36-Blocking Antibody, Is Effective for Unleashing Antitumor Immunity Against Liver Cancer and Liver Metastasis.

Project description: Not available

| S-EPMC7617665 | biostudies-literature

CD36 aggravates ferroptosis in NK cells and dampens their anti-fibrotic activity in the liver

Project description:Liver fibrosis is a major global health challenge, and it is an independent risk factor for the development of hepatocellular carcinoma (HCC). Several methods have been explored to improve liver fibrosis progression, but effective preventive and therapeutic strategies remain limited. Natural killer (NK) cells can limit the activation of hepatic stellate cells (HSCs), but they have exhibited impaired antifibrotic properties in liver fibrosis, and the underlying mechanisms are not well understood. In this study, we found that CD36 was markedly upregulated in NK cells from mice with liver fibrosis. The CD36 expression was negatively correlated with activation markers of NK cells. The CD36⁻ NK cells exhibited elevated cytotoxic cytokine production and enhanced antifibrotic activity against HSCs. The adoptive transfer of CD36⁻ NK cells alleviated liver fibrosis progression. Mechanistically, CD36 induced reactive oxygen species (ROS) and lipid peroxidation. These consequently triggered ferroptosis in NK cells. The blockage of CD36 or inhibition of ferroptosis in NK cells effectively restored their antifibrotic properties against HSCs. In summary, our findings demonstrated that the antifibrotic properties of NK cells were regulated by CD36. These results provide evidence that targeting CD36 could restore NK cell function for liver fibrosis immunotherapy.

2026-06-03 | GSE330049 | GEO

Analysis of Wild Type and hepatocyte-specific CD36 knockout (CD36LKO) mice liver Transcriptomes under high fat diet (HFD)

Project description:We generated hepatocyte-specific CD36 knockout (CD36LKO) mice to study in vivo effects of CD36 on de novo lipogenesis (DNL) under high fat diet (HFD). Lipid deposition and DNL were analyzed in primary hepatocytes isolated from CD36LKO mice or HepG2 cells with CD36 overexpression. RNA-sequence, co-immunoprecipitation and proximity ligation assay were carried out to determine its role in regulating DNL. Results: Hepatic CD36 expression was upregulated in NAFLD mice and patients, and CD36LKO mice exhibited attenuated HFD-induced hepatic steatosis and insulin resistance. We identified hepatocyte CD36 as a key regulator for DNL in the liver. Sterol regulatory element-binding protein 1 (SREBP1) and its downstream lipogenic enzymes such as FASN, ACCα and ACLY were significantly downregulated in the liver of HFD-fed CD36LKO mice, whereas overexpression CD36 stimulated insulin-mediated DNL and lipid droplet formation in vitro. Mechanistically, CD36 was activated by insulin and formed a complex with insulin induced gene-2 (INSIG2), that disrupts the interaction between SREBP cleavage-activating protein (SCAP) and INSIG2, thereby leading to the translocation of SREBP1 from ER to Golgi for processing. Furthermore, treatment with 25-hydroxycholesterol or betulin, molecules shown to enhance SCAP/INSIG interaction, reversed the effects of CD36 on SREBP1 cleavage.

2022-01-03 | GSE191059 | GEO

Lipid influx enforces liver regeneration through the recruitment of CD36+ macrophages (scRNA-Seq and RNA-Seq)

Project description:The liver possesses a remarkable regeneration capacity under a wide variety of injury conditions, like partial hepatectomy (PHx) and over-dose acetaminophen (APAP) treatment. Macrophages, multitask at the wound site by facilitating wound debridement and producing chemokines, metabolites and growth factors, and consequently determine the balance between ongoing damage and repair following tissue injury. CD36, which is universally expressed in a wide variety of cells (i.e., macrophages, adipocytes, myocytes, enterocytes and hepatocytes), and serves as the predominant fatty acid uptake facilitator of the cells to uptake microenvironmentally enriched lipids in various settings. However, the role for macrophage CD36 in mediating lipid accumulation as well as the regeneration of liver post physiological or pathophysiological injury still remains largely unknown. Herein, by utilizing multiple seq-based methods, we found the transient lipid accumulation in injured livers post PHx or APAP treatment exerted fundamental impacts on hepatic immune remodeling and induced the recruitment of macrophages with high level of CD36 expression and excessive lipid accumulation which facilitate the regeneration of livers. CD36-mediated lipid influx in macrophages triggers the activation of IRE1a signaling pathways via intracellular ceramide accumulation to promote high levels of IL6 production to accelerate liver regeneration.

2026-01-22 | GSE263879 | GEO

AMSC CD36+ subpopulations

Project description:AMSC CD36+ subpopulations

| PRJNA783325 | ENA

Unleashing Type-2 Dendritic Cells

Project description:Unleashing Type-2 Dendritic Cells

| PRJNA517156 | ENA

Study on the Mechanism of Action of Hippuric Acid Targeting the UGDH/FOXK1/CD36 Signaling Axis in Regulating Metabolic Dysfunction-AssociatedSteatotic Liver Diseases

Project description:Metabolic dysfunction-associated steatotic liver diseases (MASLD) is the most prevalent chronic liver disease globally, and the systemic metabolic disorders it triggers have become a serious public health concern. The endogenous metabolite hippuric acid (HA) is closely associated with a variety of metabolic disorders, but its molecular mechanisms in the progression of MASLD are not yet clear. Preliminary studies of this project have found that serum HA levels are significantly reduced in obese individuals and animals, and exogenous HA supplementation can alleviate body weight and liver fat accumulation in obese mice. It was also discovered that HA can reduce intracellular lipid deposition in hepatocytes by inhibiting CD36 expression. Mechanistic studies have revealed that HA can target UGDH, enhancing its binding with the transcription factor FOXK1, and inhibiting FOXK1 expression significantly reduces the transcription level of CD36. Therefore, the scientific hypothesis is proposed: HA inhibits liver fat accumulation by regulating the UGDH/FOXK1/CD36 signaling axis. This project will combine clinical sample analysis with in vitro and in vivo experiments to systematically elucidate the molecular mechanisms by which HA targets UGDH to inhibit nuclear expression of FOXK1, thereby regulating CD36 transcription. This will enhance our understanding of HA's role in lipid metabolism regulation and the development of MASLD and lay a theoretical foundation for uncovering effective therapeutic targets for MASLD.

2026-03-11 | GSE299406 | GEO

AMSC CD36+ subpopulations

Project description:Adipose-derived MSCs (AMSC) are currently utilized in clinical trials for various diseases including osteoarthritis, amyotrophic lateral sclerosis, and multiple system atrophy. Whilst AMSCs may be defined by the surface expression of classical markers including CD44, CD90, CD105, and absence of CD45, these cells may exhbit donor-to-donor differences in differentiation potential. In this study we evaluated the expression of CD36 amongst AMSCs and utilized magnetic cell sorting to enrich for CD36+ cells. Whole transcriptome RNA-sequencing was performed on unsorted, CD36+ enriched, and CD36+ depleted cells to determine gene expression difference between these populations of cells. CD36 sorted or unsorted cells were then plated and maintained in growth medium. Cells were expanded for 2 passages and passage 8 cells were plated for RNA-sequencing analysis. Trizol reagent was used to harvest cells when they were proliferating cells (~80%) or 100% confluent cells.

2021-11-28 | GSE189525 | GEO

Bulk RNA sequencing of CD36⁺ and CD36⁻ cells isolated from hiPSC-derived airway epithelial cells

Project description:To investigate whether CD36 can serve as a reliable surface marker for isolating deuterosomal cells from human induced pluripotent stem cell (hiPSC)-derived airway epithelial cells, we sorted CD36-positive and CD36-negative populations at an early stage of differentiation and performed bulk RNA sequencing. CD36⁺ cells were highly enriched for deuterosomal and multiciliated cell markers

2026-03-19 | GSE299246 | GEO

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