The DOI matches its Crossref record; 46 of the 47 references it cites were found in a registry or an index.
A mouse model of HIES reveals pro- and anti-inflammatory functions of STAT3
Open accessAbstract
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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In the citing paper
“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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Citations
Cites
Transforming growth factor-β induces development of the TH17 lineage
Mangan, P. R., Harrington, L. E., O'Quinn, D. B., Helms, W. S., Bullard, D. C., Elson, C. O., Hatton, R. D., Wahl, S. M., Schoeb, T. R., & Weaver, C. T. (2006) · Nature · doi:10.1038/nature04754 · Cited by 3,087
Interleukin-22 mediates early host defense against attaching and effacing bacterial pathogens
Zheng, Y., Valdez, P. A., Danilenko, D. M., Hu, Y., Susan, M. L., Gong, Q., Abbas, A. R., Modrusan, Z. D., Ghilardi, N., de Sauvage, F. J., et al. (2008) · Nature Medicine · doi:10.1038/nm1720 · Cited by 1,972
JAKS AND STATS: Biological Implications
Leonard, W. J., & O’Shea, J. J. (1998) · Annual Review of Immunology · doi:10.1146/annurev.immunol.16.1.293 · Cited by 1,826
Self-citationSTAT3 Regulates Cytokine-mediated Generation of Inflammatory Helper T Cells
Yang, X. O., Panopoulos, A. D., Nurieva, R., Chang, S. H., Wang, D., Watowich, S. S., & Dong, C. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.c600321200 · Cited by 1,530
Interleukin-2 Signaling via STAT5 Constrains T Helper 17 Cell Generation
Laurence, A., Tato, C. M., Davidson, T. S., Kanno, Y., Chen, Z., Yao, Z., Blank, R. B., Meylan, F., Siegel, R., Hennighausen, L., et al. (2007) · Immunity · doi:10.1016/j.immuni.2007.02.009 · Cited by 1,507
Self-citationTargeted disruption of the mouse Stat3 gene leads to early embryonic lethality
Takeda, K., Noguchi, K., Shi, W., Tanaka, T., Matsumoto, M., Yoshida, N., Kishimoto, T., & Akira, S. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.8.3801 · Cited by 1,323
STAT3 Mutations in the Hyper-IgE Syndrome
Holland, S. M., DeLeo, F. R., Elloumi, H. Z., Hsu, A. P., Uzel, G., Brodsky, N. N., Freeman, A. F., Demidowich, A. P., Davis, J., Turner, M. L. C., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa073687 · Cited by 1,233
Self-citationTakeda, K., Clausen, B. E., Kaisho, T., Tsujimura, T., Terada, N., Förster, I., & Akira, S. (1999) · Immunity · doi:10.1016/s1074-7613(00)80005-9 · Cited by 1,220
Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome
Milner, J. D., Brenchley, J. M., Laurence, A., Freeman, A. F., Hill, B. J., Elias, K. M., Kanno, Y., Spalding, C., Elloumi, H. Z., Paulson, M. L., et al. (2008) · Nature · doi:10.1038/nature06764 · Cited by 1,157
Self-citationDominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome
Minegishi, Y., Saitō, M., Tsuchiya, S., Tsuge, I., Takada, H., Hara, T., Kawamura, N., Ariga, T., Pašić, S., Stojković, O., et al. (2007) · Nature · doi:10.1038/nature06096 · Cited by 1,075
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1 of the 47 references couldn’t be matched to a known paper.
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The JAK-STAT Pathway: Impact on Human Disease and Therapeutic Intervention
O’Shea, J. J., Schwartz, D. M., Villarino, A. V., Gadina, M., McInnes, I. B., & Laurence, A. D. J. (2015) · Annual Review of Medicine · doi:10.1146/annurev-med-051113-024537 · Cited by 1,670
Self-citationMechanisms and consequences of Jak–STAT signaling in the immune system
Villarino, A. V., Kanno, Y., & O'Shea, J. J. (2017) · Nature Immunology · doi:10.1038/ni.3691 · Cited by 1,221
Self-citationHillmer, E. J., Zhang, H., Li, H. S., & Watowich, S. S. (2016) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2016.05.001 · Cited by 740
Paternoster, L., Kemp, J. P., Zheng, J., Smith, G. D., Relton, C. L., Evans, D. M., McArdle, W. L., Henderson, A. J., Standl, M., Tiesler, C. M. T., et al. (2015) · Nature Genetics · doi:10.1038/ng.3424 · Cited by 620
Mechanisms of Jak/STAT Signaling in Immunity and Disease
Villarino, A. V., Kanno, Y., Ferdinand, J. R., & O’Shea, J. J. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1401867 · Cited by 564
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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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