Essential role of Stat6 in IL-4 signalling
Abstract
Interleukin-4 (IL-4) is a pleiotropic lymphokine which plays an important role in the immune system. IL-4 activates two distinct signalling pathways through tyrosine phosphorylation of Stat6, a signal transducer and activator of transcription, and of a 170K protein called 4PS. To investigate the functional role of Stat6 in IL-4 signalling, we generated mice deficient in Stat6 by gene targeting. We report here that in the mutant mice, expression of CD23 and major histocompatibility complex (MHC) class II in resting B cells was not enhanced in response to IL-4. IL-4 induced B-cell proliferation costimulated by anti-IgM antibody was abolished. The T-cell proliferative response was also notably reduced. Furthermore, production of Th2 cytokines from T cells as well as IgE and IgG1 responses after nematode infection were profoundly reduced. These findings agreed with those obtained in IL-4 deficient mice or using antibodies to IL-4 and the IL-4 receptor. We conclude that Stat6 plays a central role in exerting IL-4 mediated biological responses.
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All of the other STAT knock-outs have relatively mild phenotypes correlated with rather specific defects in response to certain cytokines or growth factors.
“All of the other STAT knock-outs have relatively mild phenotypes correlated with rather specific defects in response to certain cytokines or growth factors (12”
From STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration (2002) · cites this paper as [36]
STAT1 and IRF5 are involved in M1 polarization/maintenance; STAT6, IRF4, CREB-C/EBPβ, and PPARγ are involved in M2 polarization/maintenance.
“Specifically, STAT1 and IRF5 have been shown to be involved in polarization and maintenance of an M1 phenotype while STAT6, IRF4, CREB-C/EBPβ, and PPARγ are involved in polarization and maintenance of an M2 phenotype [23–30].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [26]
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References 28 · Cited by 1,557
- Authors
- Takeda, K., Tanaka, T., Shi, W., Matsumoto, M., Minami, M., Kashiwamura, S.-I., Nakanishi, K., Yoshida, N., Kishimoto, T., & Akira, S.
- Affiliations
- Osaka University Hospital (JP)
- The University of Osaka (JP)
- Hyogo Medical University (JP)
- Osaka Women's and Children's Hospital (JP)
- Venue
- Nature
- Published
- 1996-04
- Volume
- 380
- Issue
- 6575
- Pages
- 627-630
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2001713238
- Cited by
- 1,557
- References
- 28
- Citations by year
- 2026: 19 · 2025: 24 · 2024: 33 · 2023: 34 · 2022: 18 · 2021: 39 · 2020: 32 · 2019: 29 · 2018: 20 · 2017: 43 · 2016: 33 · 2015: 33 · 2014: 40 · 2013: 44 · 2012: 40
- FWCI
- 44.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Amgen
- Oesterreichische Nationalbank
- National Institutes of Health
- National Institute of Mental Health
- National Institute of General Medical Sciences
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- STAT6, 4P, STAT6-deficient mice, B cell proliferation, CD23, MHC class II, T cell proliferation, Th2 cytokines, IgE, IgG1, nematode infection, IL-4 receptor, tyrosine phosphorylation
- MeSH terms
- Animals, Antibodies, Helminth, Histocompatibility Antigens Class II, B-Lymphocytes, Cell Line, Cells, Cultured, T-Lymphocytes, Helper-Inducer, Immunoglobulin A, Immunoglobulin E, Immunoglobulin G, Lymphocyte Activation, Nippostrongylus, Spleen, T-Lymphocytes, Signal Transduction, Trans-Activators, Interleukin-4, Cytokines, Receptors, IgE, Immunoglobulin Class Switching, Gene Targeting, STAT6 Transcription Factor, Mice
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