The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
STAT3 deletion during hematopoiesis causes Crohn’s disease-like pathogenesis and lethality: a critical role of STAT3 in innate immunity
Open accessAbstract
Signal transducer and activator of transcription 3 (STAT3) is a key transcriptional mediator for many cytokines and is essential for normal embryonic development. We have generated a unique strain of mice with tissue-specific disruption of STAT3 in bone marrow cells during hematopoiesis. This specific STAT3 deletion causes death of these mice within 4-6 weeks after birth with Crohn's disease-like pathogenesis in both the small and large intestine, including segmental inflammatory cell infiltration, ulceration, bowel wall thickening, and granuloma formation. Deletion of STAT3 causes significantly increased cell autonomous proliferation of cells of the myeloid lineage, both in vivo and in vitro. Most importantly, Stat3 deletion during hematopoiesis causes overly pseudoactivated innate immune responses. Although inflammatory cytokines, including tumor necrosis factor alpha and IFN-gamma, are overly produced in these mice, the NAPDH oxidase activity, which is involved in antimicrobial and innate immune responses, is inhibited. The signaling responses to lipopolysaccharide are changed in the absence of STAT3, leading to enhanced NF-kappa B activation. Our results suggest a model in which STAT3 has critical roles in the development and regulation of innate immunity, and deletion of STAT3 during hematopoiesis results in abnormalities in myeloid cells and causes Crohn's disease-like pathogenesis.
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“Impaired myeloid cells resulting in Crohn’s disease-like pathology”
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 Welte et al., 2003
In the citing paper
“STAT3-deficient macrophages, neutrophils, and DCs”
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 Welte et al., 2003
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STATs in cancer inflammation and immunity: a leading role for STAT3
Yu, H., Pardoll, D., & Jove, R. (2009) · Nature reviews. Cancer · doi:10.1038/nrc2734 · Cited by 4,383
The STATs of cancer — new molecular targets come of age
Yu, H., & Jove, R. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1275 · Cited by 2,278
Crosstalk between cancer and immune cells: role of STAT3 in the tumour microenvironment
Yu, H., Kortylewski, M., & Pardoll, D. M. (2006) · Nature reviews. Immunology · doi:10.1038/nri1995 · Cited by 1,841
Kaser, A., Zeissig, S., & Blumberg, R. S. (2010) · Annual Review of Immunology · doi:10.1146/annurev-immunol-030409-101225 · Cited by 1,806
Regulation of immune responses by L-arginine metabolism
Bronte, V., & Zanovello, P. (2005) · Nature Reviews Immunology · doi:10.1038/nri1668 · Cited by 1,775
Metadata
- Authors
- Welte, T., Zhang, S. S. M., Wang, T., Zhang, Z., Hesslein, D. G. T., Yin, Z., Kano, A., Iwamoto, Y., Li, E., Craft, J. E., Bothwell, A. L. M., Fikrig, E., Koni, P. A., Flavell, R. A., & Fu, X.-Y.
- Affiliations
- Howard Hughes Medical Institute (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-02-05
- Volume
- 100
- Issue
- 4
- Pages
- 1879-1884
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC149927
- OpenAlex
- W2148996267
- Cited by
- 381
- References
- 44
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 3 · 2023: 6 · 2022: 4 · 2021: 12 · 2020: 14 · 2019: 16 · 2018: 8 · 2017: 14 · 2016: 19 · 2015: 15 · 2014: 25 · 2013: 24 · 2012: 19
- FWCI
- 12.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Österreichischen Akademie der Wissenschaften
- National Institutes of Health (5r01ar044906-05)
- National Institute of Allergy and Infectious Diseases (AI-34522, R01AI034522)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR44906)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- STAT3, Crohn's disease, hematopoiesis, bone marrow, innate immunity, myeloid cell proliferation, intestinal inflammation, NF-κB activation, lipopolysaccharide signaling, TNF-α, interferon-gamma, granuloma formation, tissue-specific gene deletion
- MeSH terms
- Animals, Bone Marrow Cells, Cells, Cultured, Crohn Disease, DNA-Binding Proteins, Hematopoiesis, Immunity, Trans-Activators, Gene Deletion, STAT3 Transcription Factor, Mice
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