The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Inflammatory disease protective R381Q IL23 receptor polymorphism results in decreased primary CD4+ and CD8+ human T-cell functional responses
Open accessAbstract
The SNP (c.1142G > A;p.R381Q) in the IL-23 receptor (IL23R) confers protection from multiple inflammatory diseases, representing one of the most significant human genetic polymorphisms in autoimmunity. We, therefore, sought to define the functional consequences of this clinically significant variant. We find that CD4+CD45RO+ and CD8+ T cells from healthy R381Q IL23R carriers show decreased IL-23–dependent IL-17 and IL-22 production relative to WT IL23R individuals. This was associated with a lower percentage of circulating Th17 and Tc17 cells. Furthermore, CD8+ T cells from R381Q IL23R individuals showed decreased IL-23–dependent expansion and signal transducer and activator of transcription 3 (STAT3) activation compared with WT CD8+ T cells. Importantly, cells transfected with the IL23R glutamine variant show decreased IL-23–mediated signaling compared with the IL23R arginine allele. Our results show that the R381Q IL23R variant leads to selective, potentially desirable, loss of function alterations in primary human CD4+ and CD8+ T cells, resulting in highly significant protection against autoimmunity.
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Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls
The Wellcome Trust Case Control Consortium, Management Committee, Burton, P. R., Clayton, D. G., Cardon, L. R., Craddock, N., Deloukas, P., Duncanson, A., Kwiatkowski, D. P., McCarthy, M. I., et al. (2007) · Nature · doi:10.1038/nature05911 · Cited by 9,442
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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Annunziato, F., Cosmi, L., Santarlasci, V., Maggi, L., Liotta, F., Mazzinghi, B., Parente, E., Filì, L., Ferri, S., Frosali, F., et al. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070663 · Cited by 1,861
Surface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells
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Essential autocrine regulation by IL-21 in the generation of inflammatory T cells
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Interleukin-23 drives innate and T cell–mediated intestinal inflammation
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Monoclonal Anti–Interleukin 23 Reverses Active Colitis in a T Cell–Mediated Model in Mice
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Cited by
Teng, M. W. L., Bowman, E. P., McElwee, J. J., Smyth, M. J., Casanova, J.-L., Cooper, A. M., & Cua, D. J. (2015) · Nature Medicine · doi:10.1038/nm.3895 · Cited by 873
Baeten, D., Østergaard, M., Wei, J. C.-C., Sieper, J., Järvinen, P., Tam, L.-S., Salvarani, C., Kim, T.-H., Solinger, A., Datsenko, Y., et al. (2018) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2018-213328 · Cited by 390
Takagawa, T., Kitani, A., Fuss, I., Levine, B., Brant, S. R., Peter, I., Tajima, M., Nakamura, S., & Strober, W. (2018) · Science Translational Medicine · doi:10.1126/scitranslmed.aan8162 · Cited by 145
Metadata
- Authors
- Sarin, R., Wu, X., & Abraham, C.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2011-05-23
- Volume
- 108
- Issue
- 23
- Pages
- 9560-9565
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2164617201
- Cited by
- 194
- References
- 9
- FWCI
- 7.24
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Inflammatory disease protective R381Q IL23 receptor polymorphism results in decreased primary CD4+ and CD8+ human T-cell functional responses. https://app.cochat.ai/papers/10.1073/pnas.1017854108
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- Sarin, R., Wu, X., & Abraham, C. (2011). Inflammatory disease protective R381Q IL23 receptor polymorphism results in decreased primary CD4+ and CD8+ human T-cell functional responses. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1017854108
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