Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Cellular expression of PD-1, PD-L1 and CTLA-4 in patients with JAK2V617F mutated myeloproliferative disorders.

Clinical chemistry and laboratory medicine - 27 Oct 2025

Winkler Christoph, Anliker Markus, Schmidt Stefan, Feistritzer Clemens, Höchsmann Britta, Schrezenmeier Hubert, Siller Anita, Griesmacher Andrea, Loacker Lorin

Abstract excerpt

OBJECTIVES: The acquired, somatic JAK2V617F mutation is the most common molecular aberration in patients with myeloproliferative neoplasms (MPN) and also significantly involved in the regulation of T cell immunity. PD-1, PD-L1 and CTLA-4 are key immune checkpoint regulators that are elevated in patients with solid tumors, infectious diseases and chronic inflammation. We aimed further investigating the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aged
Share to B7-H1 Antigen

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to CTLA-4 Antigen

Share to CD4 gene

Share to Janus Kinase 2

Share to Mutation

Share to Myeloproliferative Disorders

Share to Programmed Cell Death 1 Receptor

Source

Identifiers

PMID: 40601823
DOI: 10.1515/cclm-2025-0306

Genes

JAK2
CD4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cellular expression of PD-1, PD-L1 and CTLA-4 in patients with JAK2V617F mutated myeloproliferative disorders.PMID 40601823Read ↗

Inflammatory Microenvironment and Specific T Cells in Myeloproliferative Neoplasms: Immunopathogenesis and Novel Immunotherapies.Semantic proximity Read ↗

Ectopic PD-L1 expression in JAK2 (V617F) myeloproliferative neoplasm patients is mediated via increased activation of STAT3 and STAT5.Semantic proximity Read ↗

Programmed death-ligand 1 expression in patients with primary or secondary myelofibrosis.Semantic proximity Read ↗

Programmed Death-Ligand 1 (PD-L1) Expression in Patients with Primary or Secondary MyelofibrosisSemantic proximity Read ↗

NK Cells in Myeloproliferative Neoplasms (MPN)Semantic proximity Read ↗

Cancer Immune Therapy for Philadelphia Chromosome-Negative Chronic Myeloproliferative NeoplasmsSemantic proximity Read ↗

Cytokine Profiling in Myeloproliferative Neoplasms: Overview on Phenotype Correlation, Outcome Prediction, and Role of Genetic Variants.Semantic proximity Read ↗

PD-L1 overexpression correlates with JAK2-V617F mutational burden and is associated with 9p uniparental disomy in myeloproliferative neoplasms.Semantic proximity Read ↗

Recent Findings in the Regulation of Programmed Death Ligand 1 ExpressionSemantic proximity Read ↗

Thrombopoietin Receptor MPL in Hematopoiesis and Myeloproliferative Neoplasms: Physiological Roles and Pathogenic Mechanisms.Semantic proximity Read ↗

Role of Next Generation Immune Checkpoint Inhibitor (ICI) Therapy in Philadelphia negative Classic Myeloproliferative neoplasm (MPN): Review of the LiteratureSemantic proximity Read ↗

Association of the composition of the bone marrow tumor microenvironment in BCR::ABL1-negative myeloproliferative neoplasms with IFN-γ signaling and driver mutations.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.