The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Distinct regulation of interleukin‐17 in human T helper lymphocytes
Open accessAbstract
Objective: Interleukin‐17 (IL‐17)–producing T helper cells have been proposed to represent a separate lineage of CD4+ cells, designated Th17 cells, which are regulated by the transcription factor retinoic acid–related orphan receptor γt (RORγt). However, despite advances in understanding murine Th17 differentiation, a systematic assessment of factors that promote the differentiation of naive human T cells to Th17 cells has not been reported. The present study was undertaken to assess the effects on naive human CD4+ T cells of cytokines known to promote murine Th17 cells. Methods: Human naive and memory CD4+ T cells isolated from peripheral blood were activated and cultured with various cytokines. Cytokine production was measured by enzyme‐linked immunosorbent assay and flow cytometry. Messenger RNA was measured by quantitative polymerase chain reaction. Results: In response to anti‐CD3/anti‐CD28 stimulation alone, human memory T cells rapidly produced IL‐17, whereas naive T cells expressed low levels. Transforming growth factor β1 and IL‐6 up‐regulated RORγt expression but did not induce Th17 differentiation of naive CD4+ T cells. However, IL‐23 up‐regulated its own receptor and was an important inducer of IL‐17 and IL‐22. Conclusion: The present data demonstrate the differential regulation of IL‐17 and RORγt expression in human CD4+ T cells compared with murine cells. Optimal conditions for the development of IL‐17–producing T cells from murine naive precursors are ineffective in human T cells. Conversely, IL‐23 promoted the generation of human Th17 cells but was also a very potent inducer of other proinflammatory cytokines. These findings may have important implications in the pathogenesis of human autoimmunity as compared with mouse models.
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Functional diversity of helper T lymphocytes
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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
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A Genome-Wide Association Study Identifies IL23R as an Inflammatory Bowel Disease Gene
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Cited by
The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing
Gaffen, S. L., Jain, R., Garg, A. V., & Cua, D. J. (2014) · Nature reviews. Immunology · doi:10.1038/nri3707 · Cited by 1,585
Generation of pathogenic TH17 cells in the absence of TGF-β signalling
Ghoreschi, K., Laurence, A., Yang, X.-P., Tato, C. M., McGeachy, M. J., Konkel, J. E., Ramos, H. L., Wei, L., Davidson, T. S., Bouladoux, N., et al. (2010) · Nature · doi:10.1038/nature09447 · Cited by 1,388
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Volpe, E., Servant, N., Zollinger, R., Bogiatzi, S. I., Hupé, P., Barillot, E., & Soumelis, V. (2008) · Nature Immunology · doi:10.1038/ni.1613 · Cited by 938
Human interleukin 17–producing cells originate from a CD161+CD4+ T cell precursor
Cosmi, L., De Palma, R., Santarlasci, V., Maggi, L., Capone, M., Frosali, F., Rodolico, G., Querci, V., Abbate, G., Angeli, R., et al. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20080397 · Cited by 706
Metadata
- Authors
- Chen, Z., Tato, C. M., Muul, L., Laurence, A., & O'Shea, J. J.
- Venue
- Arthritis & Rheumatism
- Publisher
- Wiley
- Published
- 2007-08-30
- Volume
- 56
- Issue
- 9
- Pages
- 2936-2946
- ISSN
- 0004-3591 (ISSN-L)
- 1529-0131
- OpenAlex
- W2084858972
- Cited by
- 358
- References
- 51
- FWCI
- 18.54
- Type
- journal article
- Language
- en
- Open access
- bronze
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