Cited by 381Cytokine Signaling Pathways and InteractionsInflammatory Bowel DiseasePsoriasis: Treatment and Pathogenesis

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STAT3 deletion during hematopoiesis causes Crohn’s disease-like pathogenesis and lethality: a critical role of STAT3 in innate immunity

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Welte, Thomas, Zhang, Samuel S. M., Wang, Tian, Zhang, Zhiyuan, Hesslein, David G. T., Yin, Zhinan, Kano, Arihiro, Iwamoto, Yoshiki, Li, En, Craft, Joseph E., Bothwell, Alfred L. M., Fikrig, Erol, Koni, Pandelakis A., Flavell, Richard A., Fu, Xin-Yuan·2003·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0237137100PMC PMC149927

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Abstract

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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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: Welte, Thomas
Wang, Tian
Zhang, Zhiyuan
Yin, Zhinan
Li, En
Craft, Joseph E.
Bothwell, Alfred L. M.
Fikrig, Erol
Koni, Pandelakis A.
Flavell, Richard A.
Fu, Xin-Yuan
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
DOI: 10.1073/pnas.0237137100
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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STAT3 deletion during hematopoiesis causes Crohn’s disease-like pathogenesis and lethality: a critical role of STAT3 in innate immunity

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