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SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

ABSTRACT: SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

PROVIDER: PRJNA1076213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27960535_1.fastq.gz	Fastqsanger.gz
	SRR27960535_2.fastq.gz	Fastqsanger.gz
	SRR27960536_1.fastq.gz	Fastqsanger.gz
	SRR27960536_2.fastq.gz	Fastqsanger.gz
	SRR27960537_1.fastq.gz	Fastqsanger.gz

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SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

Project description:The main challenge for immune checkpoint blockade (ICB) therapy lies in immunosuppressive tumor microenvironment (TME). Repolarizing M2-like tumor-associated macrophages (TAMs) into inflammatory M1 phenotype is a promising strategy for cancer immunotherapy. Here, we found that the transmembrane protein SHISA3 is induced by DAMPs/PAMPs in macrophages via nuclear factor-κB (NF-κB) transcription factors, and SHISA3 forms complex with HSPA8 to reciprocally activates NF-κB signaling thus maintains M1 polarization of macrophages. Enforced expression of Shisa3 in TAMs increases their phagocytosis and antigen presentation abilities and promotes CD8+ T cell-mediated antitumor immunity. Local delivery of mRNA encoding Shisa3 enables therapy of cancer by dual effects on tumor cells and TAMs, and enhance the efficacy of PD-1 antibody. Taken together, our findings describe the role of SHISA3 in reprogramming TAMs that ameliorates cancer immunotherapy To find new molecules that regulate macrophage polarization, we performed transcriptomic analysis on early macrophages polarization induced by LPS for 0, 2, 4 hours.

2024-10-02 | GSE255711 | GEO

Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

Project description:Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

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miR-15a reprograms activated hepatic stellate cells back toward quiescence

Project description:miR-15a reprograms activated hepatic stellate cells back toward quiescence

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A phosphatase-like nanomaterial promotes autophagy and reprograms macrophage for cancer immunotherapy

Project description:Macrophages are very plastic and play key roles in maintenance of tissue homeostasis. In cancer progression, macrophages also take parts through all the processes, from the initiation, progression, to the final tumor metastasis. Although energy deprivation and autophagy are widely used for cancer therapy, most of these strategies are not meant to target macrophages resulting in undesired effects and unsatisfactory outcomes for cancer immunotherapy. Herein, we developed a lanthanum nickel oxide (LNO) nanozyme that possesses phosphatase-like activity for ATP hydrolysis. Meanwhile, the autophagy of macrophages induced by LNO promotes the polarization of macrophages from M2-like macrophage (M2) to M1-like macrophage (M1) and reduces tumor-associated macrophages in tumor-bearing mice, exhibiting capability of killing tumor-associated macrophage and anti-tumor effect in vivo. Furthermore, pre-coating by myeloid cell membrane on the surface of LNO significantly enhanced antitumor immunity. Our findings demonstrate that phosphatase-like nanozyme, LNO can specifically induce macrophage autophagy that improves therapeutic efficacy and offers valuable strategies for cancer immunotherapy.

2024-08-10 | PXD051695 | Pride

Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

Project description:Dying cells release Damage-Associated Molecular Patterns (DAMPs) that can initiate and perpetuate sterile inflammatory responses. However, the effect of DAMPs on macrophages biology remains unclear. We therefore studied the effect of DAMPs on primary peritoneal macrophages (PPM) in vitro. We first performed unbiased transcriptomic profiling with RNA-seq of PPMs cultured for up to 72 hours in the presence and absence of: 1) liposaccharide (LPS), which is known to provoke an “M1” phenotype, 2) IL-4, which is known to provoke an “M2” phenotype, or 3) cytosolic extracts (CEs) from necrotic H9C2 cells to mimic the release of cardiomyocyte DAMPs. We found that the transcriptional profile of PPMs stimulated with CEs resembled the transcriptional profile of PPMs stimulated with LPS.

2019-08-21 | GSE107776 | GEO

Blocking of CA-MSC-induced desmoplasia reprograms the tumor immune microenvironment and enhances cancer immunotherapy

Project description:Blocking of CA-MSC-induced desmoplasia reprograms the tumor immune microenvironment and enhances cancer immunotherapy

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Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

Project description:Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

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Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

Project description:Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

| PRJNA1139138 | ENA

Gene expression profiling of M0, M1 and M2a macrophages after 7 days of culture

Project description:The relative contribution of polarized macrophages to the maintenance of tolerance is unknown. We examined their roles by in vivo adoptive transfer immunotherapy of M0, M1 and M2a macrophages as pre-treatment of colitis. In other experiments, M2a macrophages were used as pre-treatment or treatment of established colitis followed by immunotherapy with nTreg cells. Survival, weight gain, tissue infiltration, iTreg and Th17 cell development, T cell activation, and the frequency of proinflammatory cytokines were used as outcome measurements. Pre-treatment with M2a but not M1 macrophages increased the development of iTreg and Th17 cells. M2a macrophages used as pre-treatment or in treatment of established colitis allowed for successful therapy with nTreg cells. M1 and M2a macrophages have distinct gene expression profiles. M0, M1 and M2a macrophages were cell sorted and were used to generate total RNA for each array set, which was labeled and hybridized to Affymetrix Mouse Genome 430 2.0 GeneChips in accordance to the manufacturerâ??s protocol. Three sets of arrays were performed, and the results were averaged. The subset of probe sets whose expression increased or decreased by two-fold or more relative to M0 cells as a common standard was identified and used for further analysis.

2016-03-02 | E-GEOD-72518 | biostudies-arrayexpress

Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.

Project description:Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus. Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage. We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue. To test this hypothesis of monocyte conversion from a normal quiescent phenotype to an inflammatory phenotype, we used Affymetrix Microarray to acquire a transcriptional profile of infected monocytes at a time point our data emphasized is a key temporal regulatory point following infection. We found that HCMV significantly up-regulated 583 (5.2%) of the total genes and down-regulated 621 (5.5%) of the total genes>or=1.5-fold at 4 h postinfection. Further ontology analysis revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infection. We found that 65% of genes strictly associated with M1 polarization were up-regulated, while only 4% of genes solely associated with M2 polarization were up-regulated. Analysis of the monocyte chemokinome at the transcriptional level showed that 44% of M1 and 33% of M2 macrophage chemokines were up-regulated. Proteomic analysis using chemokine Ab arrays confirmed the secretion of these chemotactic proteins from HCMV-infected monocytes. Overall, the results identify that the HCMV-infected monocyte transcriptome displayed a unique M1/M2 polarization signature that was skewed toward the classical M1 activation phenotype.

| S-EPMC2614917 | biostudies-literature

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