ArticleThe Journal of clinical investigation2004
TYK2 is a key regulator of the surveillance of B lymphoid tumors.
Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Trial
- Cell-type-specific requirement for TYK2 in murine immune cells under steady state and challenged conditions.Cellular and molecular life sciences : CMLS · 2025Article
- The positive feedback loop of MAD2L1/TYK2/STAT3 induces progression in B-cell acute lymphoblastic leukaemia.Journal of cancer research and clinical oncology · 2023Article
- Molecular Characteristics of TYK2 Gene Expressions in Patients with Colorectal Cancer.Advanced biomedical research · 2023Article
- Consequences of sex differences in Type I IFN responses for the regulation of antiviral immunity.Frontiers in immunology · 2022Review
- Tyk2 is a tumor suppressor in colorectal cancer.Oncoimmunology · 2022Article
- Review
- Untwining Anti-Tumor and Immunosuppressive Effects of JAK Inhibitors-A Strategy for Hematological Malignancies?Cancers · 2021Review
- JAK-STAT in Early Hematopoiesis and Leukemia.Frontiers in cell and developmental biology · 2021Review
- Loss of NKG2D in murine NK cells leads to increased perforin production upon long-term stimulation with IL-2.European journal of immunology · 2020Article
- TYK2 in Tumor Immunosurveillance.Cancers · 2020Review
- STAT1 Isoforms Differentially Regulate NK Cell Maturation and Anti-tumor Activity.Frontiers in immunology · 2020Article
- Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.Leukemia · 2019Article
- NK Cells Require Cell-Extrinsic and -Intrinsic TYK2 for Full Functionality in Tumor Surveillance and Antibacterial Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- JAK/STAT Cytokine Signaling at the Crossroad of NK Cell Development and Maturation.Frontiers in immunology · 2019Review
- Compound heterozygous TYK2 mutations underlie primary immunodeficiency with T-cell lymphopenia.Scientific reports · 2018Article
- Expression of the IFNAR1 chain of type 1 interferon receptor in benign cells protects against progression of acute leukemia.Leukemia & lymphoma · 2018Article
- Germline activating TYK2 mutations in pediatric patients with two primary acute lymphoblastic leukemia occurrences.Leukemia · 2017Article
- Type I Interferons and Natural Killer Cell Regulation in Cancer.Frontiers in immunology · 2017Review
- STATs in NK-Cells: The Good, the Bad, and the Ugly.Frontiers in immunology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of the JAK-STAT pathway has been implicated in tumor formation; for example, constitutive activation of JAK2 kinase or the enforced expression of STAT5 induces leukemia in mice. We show here that the Janus kinase TYK2 serves an opposite function. Mice deficient in TYK2 developed Abelson-induced B lymphoid leukemia/lymphoma as well as TEL-JAK2-induced T lymphoid leukemia with a higher incidence and shortened latency compared with WT controls. The cell-autonomous properties of Abelson murine leukemia virus-transformed (A-MuLV-transformed) TYK2(-/-) cells were unaltered, but the high susceptibility of TYK2(-/-) mice resulted from an impaired tumor surveillance, and accordingly, TYK2(-/-) A-MuLV-induced lymphomas were easily rejected after transplantation into WT hosts. The increased rate of leukemia/lymphoma formation was linked to a decreased in vitro cytotoxic capacity of TYK2(-/-) NK and NKT cells toward tumor-derived cells. RAG2/TYK2 double-knockout mice succumbed to A-MuLV-induced leukemia/lymphoma faster than RAG2(-/-)TYK2(+/-) mice. This defines NK cells as key players in tumor surveillance in Abelson-induced malignancies. Our observations provide compelling evidence that TYK2 is an important regulator of lymphoid tumor surveillance.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.