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CCL3-Mediated Inflammatory Reprogramming of the Hepatocellular Carcinoma Microenvironment Enhances Macrophage Antigen Presentation and Adaptive Immune Response (scRNA-Seq)

ABSTRACT: CCL3-Mediated Inflammatory Reprogramming of the Hepatocellular Carcinoma Microenvironment Enhances Macrophage Antigen Presentation and Adaptive Immune Response (scRNA-Seq)

PROVIDER: PRJNA1160316 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30650775_1.fastq.gz	Fastqsanger.gz
	SRR30650775_2.fastq.gz	Fastqsanger.gz
	SRR30650776_1.fastq.gz	Fastqsanger.gz
	SRR30650776_2.fastq.gz	Fastqsanger.gz
	SRR30650777_1.fastq.gz	Fastqsanger.gz

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CCL3-Mediated Inflammatory Reprogramming of the Hepatocellular Carcinoma Microenvironment Enhances Macrophage Antigen Presentation and Adaptive Immune Response (scRNA-Seq)

Project description:Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality worldwide, largely due to its complex and immunosuppressive tumor immune microenvironment (TIME), which significantly impairs the efficacy of conventional therapies and immune checkpoint blockade (ICB). This study investigates the role of C-C motif chemokine ligand 3 (CCL3) in modulating the HCC TIME, focusing on its impact on immune cell recruitment, macrophage-mediated antigen presentation, and the overall antitumor immune response. We analyzed CCL3 expression in human HCC samples and examined its correlation with inflammatory gene signatures and immune cell infiltration. Using high-dimensional single-cell RNA sequencing (scRNA-seq), multiparameter flow cytometry, and multiplex immunofluorescence, we elucidated how CCL3 influences macrophage functionality and T cell activation. In preclinical HCC models and ex vivo tumor fragment assays, we explored the mechanisms by which CCL3 affects macrophage function and its broader implications for antitumor immunity. Our findings reveal that CCL3 effectively recruits immune cells to the HCC TIME, promotes the formation of tertiary lymphoid structures, and enhances macrophage-mediated antigen phagocytosis and presentation, leading to improved T cell effector functions and cytotoxic activity. This research underscores the critical role of CCL3 in reshaping the HCC TIME to enhance antitumor immunity and suggests that targeting CCL3 could be a promising strategy to improve the efficacy of immunotherapy in liver cancer.

2025-03-05 | GSE277066 | GEO

CCL3-Mediated Inflammatory Reprogramming of the Hepatocellular Carcinoma Microenvironment Enhances Macrophage Antigen Presentation and Adaptive Immune Response (RNA-Seq)

2025-03-03 | GSE277065 | GEO

CCL3-Mediated Inflammatory Reprogramming of the Hepatocellular Carcinoma Microenvironment Enhances Macrophage Antigen Presentation and Adaptive Immune Response (RNA-Seq)

Project description:CCL3-Mediated Inflammatory Reprogramming of the Hepatocellular Carcinoma Microenvironment Enhances Macrophage Antigen Presentation and Adaptive Immune Response (RNA-Seq)

| PRJNA1160314 | ENA

Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Antigen Presentation and Immunogenicity [bulk RNA-seq]

Project description:Loss of antigen presentation by MHCI is a common mechanism of tumor immune evasion. Mitochondrial oxidative phosphorylation (OXPHOS) capacity influences MHCI expression, but the underlying molecular mechanisms remain unclear. Here, we demonstrate that the relative flow of electrons through complex I or II of the mitochondrial electron transport chain (ETC) regulates MHCI expression and antigen presentation in cancer cells. Specifically, reducing electron flow from complex II increases mitochondrial succinate which activates transcription of MHCI and antigen processing and presentation (APP) genes. These phenotypes are independent of the interferon (IFN) signaling pathway and driven by succinate-mediated enzymatic inhibition of lysine-specific demethylases, KDM5A/B and destabilization of polycomb repressor complex 2 (PRC2). Finally, knockout of the mitochondrial Complex I inhibitor protein, MCJ, preferentially reduces electron flow through Complex II and increases succinate which drives an enhanced antigen-dependent CD8+ T cell response to mouse melanoma tumors in vivo. These findings suggest that the mitochondrial ETC can be manipulated therapeutically to enhance antitumor immune responses independently of IFNγ.

2022-12-31 | GSE198346 | GEO

Oligomeric human Aβ1-42 inhibits antigen presentation

Project description:Oligomeric human Aβ1-42 inhibits antigen presentation

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Atractylenolide I enhances responsiveness to immune checkpoint blockade therapy by activating tumor antigen presentation

Project description:One of the primary mechanisms of tumor cell immune evasion is the loss of antigenicity, which arises due to lack of immunogenic tumor antigens as well as dysregulation of the antigen processing machinery. In a screen for small-molecule compounds from herbal medicine thatpotetiate T cell-mediated cytotoxicity, we identified atractylenolide I (ATT-I) that significantly promotes tumor antigen presentation of both human and mouse colorectal cancer (CRC) cells and thereby enhances the cytotoxic response of CD8+ T cells. Cellular thermal shift assay (CETSA) with multiplexed quantitative mass spectrometry identified the proteasome 26S subunit non-ATPase 4 (PSMD4), an essential component of the immunoproteasome complex,as a primary target protein of ATT-I. Binding of ATT-I with PSMD4 augments the antigenprocessing activity of immunoproteasome, leading to enhanced major histocompatibility class I(MHC-I)-mediated antigen presentation on cancer cells. In syngeneic mouse CRC models and human patient-derived CRC organoid models, ATT-I treatment promotes the cytotoxicity of CD8+ T cells and thus profoundly enhances the efficacy of immune checkpoint blockade therapy. Collectively, we show here that targeting the function of immunoproteasome with ATT-I promotes tumor antigen presentation, empowers T-cell cytotoxicity, and thus elevates the tumorresponse to immunotherapy.

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Increased antigen cross-presentation but impaired cross-priming after activation of PPARÎ³

Project description:Increased antigen cross-presentation but impaired cross-priming after activation of PPARÎ³ is mediated by up-regulation of B7H1 Dendritic cells (DCs) are able to take up exogenous antigens and present antigen-derived peptides on MHC class I molecules, a process termed cross-presentation. The mannose receptor (MR), an endocytic receptor expressed on a variety of antigen-presenting cells (APCs), has been demonstrated to target soluble antigens exclusively towards cross-presentation. In this study, we investigated the role of the murine nuclear receptor peroxisome proliferator-activated receptor Î³ (PPARÎ³), a ligand-activated transcription factor with immunomodulatory properties, in MR-mediated endocytosis and cross-presentation of the model antigen ovalbumin (OVA). We could demonstrate both in vitro and in vivo that activation of PPARÎ³ resulted in increased MR expression, which in consequence led to enhanced MR-mediated endocytosis and elevated cross-presentation of soluble OVA. Concomitantly, activation of PPARÎ³ in DCs induced up-regulation of the co-inhibitory molecule B7H1, which, despite enhanced cross-presentation, caused an impaired activation of naive OVA-specific CD8+ T cells and the induction of T cell tolerance. These data provide a mechanistic basis for the immunomodulatory action of PPARÎ³ which might open new possibilities in development of therapeutical approaches aimed at the control of excessive immune responses, e.g. in T cell-mediated autoimmunity. Comparison of murine mannose receptor negative versus mannose receptor positive bone marrow-derived DCs

2010-05-08 | E-GEOD-15616 | biostudies-arrayexpress

Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Antigen Presentation and Immunogenicity

Project description:Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Antigen Presentation and Immunogenicity

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Allogeneic red blood cell transfusion impairs antigen presentation and stimulates inflammatory response

Project description:Allogeneic red blood cell transfusion increases risk of infection and organ injury, which we here attempted to explain by analyzing gene expression in various types of immune cells. We prospectively compared adverse events and transcriptomic profiles in immune cells between patients who received transfusion of red blood cells (not plasma or platelets) during or after on-pump cardiac surgery and patients who did not. The composite rate of adverse events was significantly more frequent among patients who received transfusions (4 of 16, 25%) than among those who did not (3 of 60, 5%, p = 0.03). Transfusion downregulated in monocytes several genes involved in antigen presentation, such as HLA-DQA2 and HLA-DPB1, as well as several ligand-receptor pairs linking monocytes to natural killer cells (HLA-C-KIR2DL1, HLA-E-CD94:NKG2A) and T cells (CD28-CD86, CD2-CD58) for antigen presentation. Transfusion upregulated the early activation marker CD69 and pro-inflammatory and chemotactic factors (IL-6, TNFR1, TNFR2, CXCL9 and CCL3) in T, B and natural killer cells. Transfusion volume correlated positively with the percentage of CD69+ CD8+ T cells, which in turn correlated positively with composite risk of adverse events. Our findings may help explain how transfusion causes immunosuppression and systemic inflammation, thereby increasing risk of adverse events. Our work may provide clues to developing preventive or mitigating measures in order to optimize prognosis of patients who receive blood cell transfusions.

2025-03-19 | GSE251696 | GEO

HLA-DM allotypes - Distinct editing functions of natural HLA-DM allotypes impact antigen presentation and CD4+ T cell activation

Project description:Major Histocompatibility Complex of Class II (MHCII) antigen presentation is a key event of adaptive immunity. HLA-DM favors the presentation of kinetically stable peptide-MHCII complexes but does not bind peptides itself and exhibits only a low degree of polymorphism. To date, no evidence for altered function of DM due to natural variations has been reported. We define the presence of DM haplotypes in human populations covered by the 1000 Genomes Project and probe their activity in antigen presentation assays. Our results indicate a clear linkage between DMA*0103 and DMB*0107 never reported before. Thehe corresponding heterodimer features a distinct activity profile when compared to the most frequent allotype (DMA*0101-DMB*0101). In vitro experiments demonstrate a broader pH activity profile for the new allotype, explaining its characteristic cellular function. Together, our results suggest that natural variations of DM have important consequences for an individual’s adaptive immune response.

2018-10-31 | PXD009791 | Pride

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