JAKs and STATs in immunity, immunodeficiency, and cancer
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A large number of cytokines signal through the JAK–STAT pathway. Abnormal function of this pathway may lead to a variety of diseases. Targeting the defects in this signaling pathway has already led to treatment advances, and further advances are likely.
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The JAK/STAT pathway is activated by many protein ligands, including cytokines, growth factors, interferons, and peptide hormones, and regulates cell growth, proliferation, differentiation, and apoptosis.
“This pathway is activated in response to many protein ligands, including cytokines, growth factors, interferons (IFNs), and peptide hormones, where it regulates a wide range of cellular processes, including cell growth, proliferation, differentiation, and apoptosis (Rawlings et al., 2004; O’Shea et al., 2013).”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as O’Shea et al., 2013
The CYTOKINES AND JAK–STAT SIGNALING section identifies interferons, colony-stimulating factors, growth hormone, and other peptide hormones as ligands whose receptors use JAK–STAT signaling, and links these signals to growth and differentiation. The CANCER section links STAT activation to proliferation and cell survival. The source does not support the implication that growth factors generally activate this pathway, and it does not explicitly describe apoptosis as a process the pathway regulates. (LLM, conf=0.86)
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“This pathway is activated in response to many protein ligands, including cytokines, growth factors, interferons (IFNs), and peptide hormones, where it regulates a wide range of cellular processes, including cell growth, proliferation, differentiation, and apoptosis (Rawlings et al., 2004; O’Shea et al., 2013).”
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- Authors
- O'Shea, J. J., Holland, S. M., & Staudt, L. M.
- Affiliations
- National Institute of Allergy and Infectious Diseases (US)
- National Institutes of Health (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2013-01-10
- Volume
- 368
- Issue
- 2
- Pages
- 161-170
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC7604876
- OpenAlex
- W2040002852
- Cited by
- 927
- References
- 101
- Citations by year
- 2026: 47 · 2025: 61 · 2024: 64 · 2023: 76 · 2022: 79 · 2021: 91 · 2020: 78 · 2019: 60 · 2018: 44 · 2017: 70 · 2016: 66 · 2015: 69 · 2014: 67 · 2013: 52
- FWCI
- 8.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (Z01SC004024)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (ZIAAR041106)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- JAK/STAT signaling, cytokine signaling, immunodeficiency, cancer, immune regulation, JAK inhibitors, STAT inhibitors, targeted therapy
- MeSH terms
- Hematologic Diseases, Humans, Immunologic Deficiency Syndromes, Mutation, Neoplasms, Signal Transduction, Cytokines, STAT Transcription Factors, Janus Kinases
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