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Cholestasis-induced neutrophil phenotypic transformation contributes to the immune escape of colorectal liver metastasis

ABSTRACT: Cholestasis-induced neutrophil phenotypic transformation contributes to the immune escape of colorectal liver metastasis

PROVIDER: PRJNA862549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20656923_1.fastq.gz	Fastqsanger.gz
	SRR20656923_2.fastq.gz	Fastqsanger.gz
	SRR20656924_1.fastq.gz	Fastqsanger.gz
	SRR20656924_2.fastq.gz	Fastqsanger.gz
	SRR20656925_1.fastq.gz	Fastqsanger.gz

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Cholestasis-induced neutrophil phenotypic transformation contributes to the immune escape of colorectal liver metastasis

Project description:Cholestasis, a serious complication of liver metastasis (LM), contributes to dismal prognosis in patients with colorectal cancer and LM. However, the mechanism underlying the effect of cholestasis on the development of LM or pre-metastatic microenvironment in the liver remains elusive. In this study, we discovered that cholestasis accelerated the progression of LM and is associated with increased neutrophil infiltration, T-cell exclusion, and exhaustion. Besides, Tβ-MCA and GCA promoted the expression of Arg1 and iNOS in neutrophils via the p38/MAPK signaling pathway. The significant suppression of the activation and cytotoxic effects of CD8+ T cells during co-culture with BA-pretreated neutrophils indicated that BAs directly induce the polarization of immunosuppressive neutrophils. Importantly, targeting BA anabolism with Obeticholic acid effectively suppressed the LM of colorectal cancer in a cholestasis mouse model. Our findings suggest that cholestasis, associated with the failure to achieve drainage of primary BAs, accelerates the progression of LM by remodeling the tumor immune microenvironment. Moreover, targeting BA anabolism with OCA may represent a therapeutic strategy for cholestasis-associated LM of colorectal cancer.

2024-07-10 | GSE209836 | GEO

T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants

Project description:T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants

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T cell Immune Escape in Blast Crisis Transformation of Chronic Myeloid Leukemia

Project description:T cell Immune Escape in Blast Crisis Transformation of Chronic Myeloid Leukemia

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Discrimination of etiologically different cholestasis by modeling proteomics datasets

Project description:Cholestasis is characterized by disrupted bile flow from the liver to the small intestine. Although etiologically different cholestasis display similar symptoms, diverse factors can contribute to the progression of the disease and determines the appropriate therapeutic option. Therefore, stratifying cholestatic patients is essential for the development of tailor-made treatment strategies. Here, we have analyzed the liver proteome from cholestatic patients of different etiology. 7,161 proteins were identified and quantified, of which 263 were differentially expressed between control and cholestasis groups. These differential proteins point to deregulated cellular processes that explain part of the molecular framework of cholestasis progression. However, the clustering of different cholestasis types was limited. Therefore, a machine learning pipeline was designed to identify a panel of 20 differential proteins that segregate different cholestasis groups with high accuracy and sensitivity. In summary, proteomics combined with machine learning algorithms provides valuable insights into the molecular mechanisms of cholestasis progression and a panel of proteins to discriminate across different types of cholestasis. This strategy may prove useful to develop precision medicine approaches for patient care.

2024-05-22 | PXD047823 | Pride

T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants [scRNA-Seq]

Project description:T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants [scRNA-Seq]

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T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants [bulk RNA-seq]

Project description:T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants [bulk RNA-seq]

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T cell Immune Escape in Blast Crisis Transformation of Chronic Myeloid Leukemia

Project description:Chronic myeloid leukemia (CML) may transform from a chronic phase (CP) into blast crisis (BC), which is often incurable. Herein, we report that miR-142 deficit acquired by T lymphocytes contributes to BC transformation by promoting immune escape. We observe that T cells of BC patients lack miR-142 and are fewer and exhausted compared with CP patients. Similarly, BC miR-142−/−/BCR/ABL+/+ mouse presents with T lymphopenia compared with the CP miR-142+/+/BCR/ABL+/+ mouse. In the BC mouse, miR-142 deficit impairs thymic differentiation of lymphoid-primed multipotent progenitors (LMPP) into mature T cells and redirects them toward myeloid lineage. The fewer mature T cells in the BC mouse are enriched with exhausted T effectors. MiR-142 deficit, driven by leukemic blasts-secreted inflammatory cytokines (i.e., IL-6), induces T cell hypofunction by preventing the metabolic reprogramming that allows activated T cells to thrive and expand. This ultimately results in an increase in T cell spontaneous apoptosis and BC immune escape. In fact, NSG mice transplanted with BC CML LSKs and miR-142 KO T cells had shorter survival than mice transplanted with BC CML LSKs and miR-142 wild-typewt T cells. Conversely, BC patient-derived xenograft (PDX) mice receiving autologous T cells and synthetic miR-142 lived longer than those receiving autologous T cells and scramble RNA. Combination of tyrosine kinase inhibitors (TKI) plus synthetic miR-142 and/or PD-1 antibody induced a prolonged survival compared to TKI alone, suggesting that harnessing the host immune system with synthetic miR-142 and immunocheckpoint inhibitors along with BCR/ABL inhibition may provide novel therapeutic opportunities.

2024-01-31 | GSE254285 | GEO

Fecal microbes in cholestasis

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Functional evaluation of neutrophil of patients at high risk for infection treated with monocyte/ neutrophil apheresis

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The protective effect of celastrol in ANIT-induced cholestasis

Project description:Purpose: The goals of this study was to (1) evaluate the protective effect of celastrol on alpha-naphthylisothiocyanate (ANIT)-induced cholestasis and (2) which genes were recovered by celastrol. Methods:To investigate the protective effect of celastrol on ANIT-induced cholestasis, the WT mice were randomly assigned into two groups, respectively (n=3): (1) ANIT; (2) ANIT+Celastrol. ANIT+Celastrol group was orally treated with celastrol (10 mg/kg dissolved in 1% DMSO + 2% Tween 80 + 97% water) for 5 consecutive days. After celastrol was treated for 3 days, ANIT and ANIT+Celastrol groups were given a single oral dose of ANIT. All mice were killed 48 h after ANIT administration. Liver samples were harvested and frozen at -80 °C before analysis. Results: A total of 978 DEGs were identified. Large numbers of these DEGs were related to activation of SIRT1, which included increased FXR signaling and inhibition of PPARγ, nuclear factor-kappa B (NF-κB), and P53 signaling. Conclusions: Celastrol could protect ANIT-induced cholestasis by recovering disrupted Sirt1 level.

2018-02-09 | GSE110391 | GEO

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