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A mouse model of HIES reveals pro- and anti-inflammatory functions of STAT3
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Key Points: Mice that express a mutation in STAT3 phenocopy patients with HIES. Bone marrow transplantation does not fully correct the susceptibility of these animals to bacterial infection.
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“Specifically, daily administration of TTI-101 for 14 days skewed T cell development away from Th17 cells toward Th1 cells, thereby phenocopying mice that transgenically express a dominant-negative STAT3 mutation (Steward-Tharp et al., 2014).”
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 Steward-Tharp et al., 2014
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“Exposure of mice to TTI-101 has modest and expected effects on T cell subsets and myeloid cells.”
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 Steward-Tharp et al., 2014
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Self-citationRegulation of the germinal center reaction by T helper cells and T regulatory cells
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Liu, J., Szilágyi, K. L., Capitano, M. L., Iyer, A. K., He, J., Olson, M. R., Du, J., Pol, W. V. D., Morrow, C. D., Zhou, B., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.07.31.453520
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AD-HIES patients retain preTh17-cells that produce IL10 with opportunistic pathogens and induce IgEPreprint
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Mouse Model of STAT3 Mutation Resulting in Job’s Syndrome Diverges from Human Pathology
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Metadata
- Authors
- Steward-Tharp, S. M., Laurence, A., Kanno, Y., Kotlyar, A., Villarino, A. V., Sciume, G., Kuchen, S., Resch, W., Wohlfert, E. A., Jiang, K., Hirahara, K., Vahedi, G., Sun, H.-W., Feigenbaum, L., Milner, J. D., Holland, S. M., Casellas, R., Powrie, F., & O'Shea, J. J.
- Affiliations
- National Institutes of Health (US)
- Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD;
- University at Buffalo, State University of New York (US)
- Laboratory of Allergic Diseases, and
- University of Oxford (GB)
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2014-05-08
- Volume
- 123
- Issue
- 19
- Pages
- 2978-2987
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC4014840
- OpenAlex
- W2056663587
- Cited by
- 87
- References
- 47
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 5 · 2021: 10 · 2020: 10 · 2019: 5 · 2018: 11 · 2017: 5 · 2016: 8 · 2015: 9 · 2014: 4
- FWCI
- 3.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Bern Open Repository and Information System (University of Bern) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Wellcome Trust (095688/Z/11/Z, 095688)
- National Institutes of Health
- Japan Society for the Promotion of Science (25893032)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- hyperimmunoglobulin E syndrome, STAT3, mouse model, hematopoietic stem cell transplantation, Th17 cells, serum IgE, bacterial infection susceptibility, epithelium, transgenic mice
- MeSH terms
- Animals, Cells, Cultured, Disease Models, Animal, Enterobacteriaceae Infections, Flow Cytometry, Humans, Immunoglobulin E, Job Syndrome, Lipopolysaccharides, Mice, Transgenic, Mutation, Shock, Septic, Survival Analysis, Bone Marrow Transplantation, Cytokines, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Citrobacter rodentium, STAT3 Transcription Factor, Mice, Host-Pathogen Interactions, Transcriptome
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