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Autoimmune arthritis associated with mutated interleukin (IL)-6 receptor gp130 is driven by STAT3/IL-7-dependent homeostatic proliferation of CD4+ T cells
Open accessAbstract
Mice homozygous for the F759 mutation in the gp130 interleukin (IL)-6 receptor subunit have enhanced gp130-mediated signal transducer and activator of transcription (STAT)3 activation and spontaneously developed a lymphocyte-mediated rheumatoid arthritis-like joint disease. Here, we show that the development of the disease is dependent on both major histocompatibility complex (MHC) II–restricted CD4+ T cells and IL-6 family cytokines. In spite of the necessity for CD4+ T cells, the gp130 mutation was only required in nonhemtopoietic cells for the disease. The gp130 mutation resulted in enhanced production of IL-7. Conditional knockout of STAT3 in nonlymphoid cells showed that the enhancement of IL-7 production was dependent on STAT3 activation by IL-6 family cytokines. Homeostatic proliferation of CD4+ T cells was enhanced in gp130 mutant mice and acceleration of homeostatic proliferation enhanced the disease, whereas the inhibition of homeostatic proliferation suppressed the disease. Anti–IL-7 antibody treatment inhibited not only the enhanced homeostatic proliferation, but also the disease in gp130 mutant mice. Thus, our results show that autoimmune disease in gp130 mutant mice is caused by increased homeostatic proliferation of CD4+ T cells, which is due to elevated production of IL-7 by nonhematopoietic cells as a result of IL-6 family cytokine-gp130-STAT3 signaling.
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“Further, they act on fibroblasts and endothelial cells to recruit T helper 17 (Th17) cells, leading to an RA-like joint disease (F759 arthritis) and experimental autoimmune encephalomyelitis (EAE) (54, 66, 99).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [99]
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“In fact, a mutated gp130-mediated excessive production of cytokines and chemokines in non-immune cells in F759 mice is necessary for CD4(+) T-cell proliferation, Th17 cell accumulation in the lesion and the arthritis development (66, 99).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [99]
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“Although the development of F759 arthritis is dependent on Th17 cells, the F759 mutation is required in non-immune cells but not immune cells, clearly indicating that the interaction between non-immune cells and immune cells is crucial for arthritis development in F759 mice (66, 99).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [99]
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“Although the development of F759 arthritis is dependent on Th17 cells, the F759 mutation is required in non-immune cells but not immune cells, clearly indicating that the interaction between non-immune cells and immune cells is crucial for arthritis development in F759 mice (66, 99).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [99]
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“We first investigated the roles of IL-17A and IL-6 signaling in fibroblasts because we previously used chimeric mice with transplanted bone-marrow cells to show that the F759 mutation in nonhematopoietic cells but not in hematopoietic cells results in spontaneous autoimmune arthritis (Sawa et al., 2006).”
BackgroundMethodInfluentialSelf-citation
Metadata
- Authors
- Sawa, S.-I., Kamimura, D., Jin, G.-H., Morikawa, H., Kamon, H., Nishihara, M., Ishihara, K., Murakami, M., & Hirano, T.
- Affiliations
- 1Laboratory of Developmental Immunology, Graduate School of Frontier Bioscience and Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
- RIKEN (JP)
- The University of Osaka (JP)
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2006-05-22
- Volume
- 203
- Issue
- 6
- Pages
- 1459-1470
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2118324
- OpenAlex
- W2133947803
- Cited by
- 176
- References
- 49
- Citations by year
- 2026: 7 · 2025: 4 · 2024: 3 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 3 · 2019: 7 · 2018: 7 · 2017: 8 · 2016: 6 · 2015: 16 · 2014: 8 · 2013: 9 · 2012: 19
- FWCI
- 6.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- autoimmune arthritis, gp130, IL-6 receptor, STAT3, IL-7, IL-6 family cytokines, MHC class II-restricted T cells, non-hematopoietic cells
- MeSH terms
- Animals, Arthritis, Autoimmune Diseases, Disease Models, Animal, Flow Cytometry, Homeostasis, Homozygote, Humans, Lymphocyte Activation, Mice, Inbred C57BL, Mutation, Thymectomy, CD4-Positive T-Lymphocytes, Interleukin-7, STAT3 Transcription Factor, Cytokine Receptor gp130, Mice
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