The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Interleukin‐17–producing T cells are enriched in the joints of children with arthritis, but have a reciprocal relationship to regulatory T cell numbers
Open accessAbstract
Objective: To identify interleukin‐17 (IL‐17)–producing T cells from patients with juvenile idiopathic arthritis (JIA), and investigate their cytokine production, migratory capacity, and relationship to Treg cells at sites of inflammation, as well as to test the hypothesis that IL‐17+ T cell numbers correlate with clinical phenotype in childhood arthritis. Methods: Flow cytometry was used to analyze the phenotype, cytokine production, and chemokine receptor expression of IL‐17–producing T cells in peripheral blood and synovial fluid mononuclear cells from 36 children with JIA, in parallel with analysis of forkhead box P3 (FoxP3)–positive Treg cells. Migration of IL‐17+ T cells toward CCL20 was assessed by a Transwell assay. Synovial tissue was analyzed by immunohistochemistry for IL‐17 and IL‐22. Results: IL‐17+ T cells were enriched in the joints of children with JIA as compared with the blood of JIA patients (P = 0.0001) and controls (P = 0.018) and were demonstrated in synovial tissue. IL‐17+ T cell numbers were higher in patients with extended oligoarthritis, the more severe subtype of JIA, as compared with patients with persistent oligoarthritis, the milder subtype (P = 0.046). Within the joint, there was an inverse relationship between IL‐17+ T cells and FoxP3+ Treg cells (r = 0.61, P = 0.016). IL‐17+,CD4+ T cells were uniformly CCR6+ and migrated toward CCL20, but synovial IL‐17+ T cells had variable CCR4 expression. A proportion of IL‐17+ synovial T cells produced IL‐22 and interferon‐γ. Conclusion: This study is the first to define the frequency and characteristics of “Th17” cells in JIA. We suggest that these highly proinflammatory cells contribute to joint pathology, as indicated by relationships with clinical phenotypes, and that the balance between IL‐17+ T cells and Treg cells may be critical to outcome.
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Cites
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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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
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Reciprocal T H 17 and Regulatory T Cell Differentiation Mediated by Retinoic Acid
Mucida, D., Park, Y., Kim, G., Turovskaya, O., Scott, I., Kronenberg, M., & Cheroutre, H. (2007) · Science · doi:10.1126/science.1145697 · Cited by 1,982
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“The requirements for the generation of human Th17 cells in the physiologic context may be more dependent on IL-6 and IL-1 (13,14), but what regulates the balance between Th17 cells and Treg cells in health or disease has not yet been fully elucidated.”
BackgroundSurface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells
Acosta-Rodriguez, E. V., Rivino, L., Geginat, J., Jarrossay, D., Gattorno, M., Lanzavecchia, A., Sallusto, F., & Napolitani, G. (2007) · Nature Immunology · doi:10.1038/ni1467 · Cited by 1,828
Cited by
Prakken, B., Albani, S., & Martini, A. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60244-4 · Cited by 771
Th17 plasticity in human autoimmune arthritis is driven by the inflammatory environment
Nistala, K., Adams, S., Cambrook, H., Ursu, S., Olivito, B., de Jager, W., Evans, J. G., Cimaz, R., Bajaj-Elliott, M., & Wedderburn, L. R. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1003852107 · Cited by 443
Self-citationThe IL-23-IL-17 axis in inflammatory arthritis
Lubberts, E. (2015) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2015.53 · Cited by 442
Cardiac myosin-Th17 responses promote heart failure in human myocarditis
Myers, J. M., Cooper, L. T., Kem, D. C., Stavrakis, S., Kosanke, S. D., Shevach, E. M., Fairweather, D., Stoner, J. A., Cox, C. J., & Cunningham, M. W. (2016) · JCI Insight · doi:10.1172/jci.insight.85851 · Cited by 230
CD161 defines the subset of FoxP3+ T cells capable of producing proinflammatory cytokines
Pesenacker, A. M., Bending, D., Ursu, S., Wu, Q., Nistala, K., & Wedderburn, L. R. (2013) · Blood · doi:10.1182/blood-2012-08-443473 · Cited by 175
Self-citationLubberts, E. (2010) · Seminars in Immunopathology · doi:10.1007/s00281-009-0189-9 · Cited by 173
Metadata
- Authors
- Nistala, K., Moncrieffe, H., Newton, K. R., Varsani, H., Hunter, P., & Wedderburn, L. R.
- Venue
- Arthritis & Rheumatism
- Publisher
- Wiley
- Published
- 2008-02-29
- Volume
- 58
- Issue
- 3
- Pages
- 875-887
- ISSN
- 0004-3591 (ISSN-L)
- 1529-0131
- OpenAlex
- W1979036381
- Cited by
- 334
- References
- 13
- FWCI
- 19.46
- Type
- journal article
- Language
- en
- Open access
- bronze
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