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Mus musculus

ABSTRACT: Clonal hematopoiesis with JAK2V617F promotes pulmonary hypertension through ALK1

PROVIDER: PRJDB9389 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR212814.fastq.gz	Fastqsanger.gz
	DRR212815.fastq.gz	Fastqsanger.gz
	DRR212816.fastq.gz	Fastqsanger.gz
	DRR212817.fastq.gz	Fastqsanger.gz
	DRR212818.fastq.gz	Fastqsanger.gz

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IL-18 Inhibition Aggravates Atherosclerosis in Jak2V617F Clonal Hematopoiesis

Project description:Clonal hematopoiesis (CH) driven by Jak2V617F is known to accelerate atherosclerosis through inflammasome activation and release of IL-1β and IL-18, yet the specific contribution of IL-18 has remained unclear. In this study, we demonstrate that antibody inhibition of IL-18 in Jak2V617F CH mice increases plaque collagen but paradoxically promotes both early lesion growth and advanced necrotic core formation. Mechanistically, IL-18 blockade reverses AIM2 inflammasome activation but shifts cell death toward apoptosis, and together with impaired efferocytosis, results in greater necrosis. These events appear to be coordinated by reduced IFN-γ signaling, which enhanced collagen deposition while decreasing expression of efferocytotic genes.Our findings challenge the prevailing notion that IL-18 inhibition stabilizes atherosclerotic plaques in CH and provide new mechanistic insight into the interplay between inflammasome biology, adaptive immunity, and plaque stability.

2025-10-30 | E-MTAB-15736 | biostudies-arrayexpress

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Impaired IL-10 Receptor Signaling Leads to Inflammation Induced Exhaustion in Hematopoietic Stem Cells

Project description:Chronic-inflammation compromises normal hematopoiesis, and interleukin-10 (IL-10) signaling is essential for restraining inflammatory responses. When inflammation persists, hematopoietic stem cells (HSCs) undergo proliferative exhaustion with loss of fitness and regenerative capacity. We previously showed that in JAK2V617F myeloproliferative neoplasm (MPN) primary monocytes exhibit impaired IL-10 signaling. Because clonal hematopoiesis is a hallmark of exhaustion, we hypothesize that impaired IL-10 signaling confers a selective advantage to clonal hematopoiesis by promoting inflammation-induced exhaustion in nonmalignant cells. We used an IL-10R blocking antibody in murine models with repeated exposure to lipopolysaccharide (LPS), an inflammatory stimulus, this showed IL-10R blockade exacerbated exhaustion phenotypes, increasing proliferation, myeloid skewing, and reduced HSC fitness relative to controls. In JAK2V617F murine models, JAK2V617F-expressing cells were not impaired by inflammatory exposure in the presence of IL-10R blockade, which in turn aggravated MPN-like phenotypes and clonal expansion. Taken together, these findings indicate that defective IL-10 receptor signaling prolongs inflammatory responses, accelerates exhaustion phenotypes, and reduces the competitiveness of normal hematopoietic clones in the context of hematologic malignancy.

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IL-18 Inhibition Aggravates Atherosclerosis in Jak2V617F Clonal Hematopoiesis

Project description:IL-18 Inhibition Aggravates Atherosclerosis in Jak2V617F Clonal Hematopoiesis

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Depletion of Jak2V617F MPN-propagating stem cells by interferon-alpha in a murine model of polycythemia vera

Project description:Interferon alpha (IFNa) is an effective treatment for patients with myeloproliferative neoplasms (MPN). In addition to inducing hematological responses in most MPN patients, IFNa reduces the JAK2V617F allelic burden and can render the JAK2V617F mutant clone undetectable in some patients. The precise mechanism underlying these responses is incompletely understood and whether the molecular responses that are seen occur due to the effects of IFNa on JAK2V617F mutant stem cells is debated. Using a murine model of Jak2V617F MPN, we investigated the effects of IFNa on Jak2V617F MPN-propagating stem cells in vivo. We report that IFNa treatment induces hematological responses in the model and causes depletion of Jak2V617F MPN-propagating cells over time, impairing disease transplantation. We demonstrate that IFNa treatment induces cell-cycle activation of Jak2V617F mutant long-term hematopoietic stem cells (LT-HSC) and promotes a predetermined erythroid-lineage differentiation program. These findings provide insights into the differential effects of IFNa on Jak2V617F mutant and normal hematopoiesis and suggest that IFNa achieves molecular remissions in MPN patients through its effects on MPN stem cells. Furthermore, these results support combinatorial therapeutic approaches in MPN, by concurrently depleting dormant JAK2V617F MPN-propagating stem cells with IFNa and targeting the proliferating downstream progeny with JAK2-inhibitors or cytotoxic chemotherapy. HSC-enriched population from WT (CD45.1) or Jak2VF knockin (CD45.2), after 4 weeks of interferon alpha or vehicle treatment. N=4 per condition

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