The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Anti–TNF-α therapy induces a distinct regulatory T cell population in patients with rheumatoid arthritis via TGF-β
Open accessAbstract
The induction of regulatory T (T reg) cells holds considerable potential as a treatment for autoimmune diseases. We have previously shown that CD4+CD25hi T reg cells isolated from patients with active rheumatoid arthritis (RA) have a defect in their ability to suppress proinflammatory cytokine production by CD4+CD25− T cells. This defect, however, was overcome after anti–tumor necrosis factor (TNF)-α antibody (infliximab) therapy. Here, we demonstrate that infliximab therapy gives rise to a CD4+CD25hiFoxP3+ T reg cell population, which mediates suppression via transforming growth factor (TGF)-β and interleukin 10, and lacks CD62L expression, thereby distinguishing this T reg cell subset from natural T reg cells present in healthy individuals and patients with active RA. In vitro, infliximab induced the differentiation of CD62L− T reg cells from CD4+CD25− T cells isolated from active RA patients, a process dependent on TGF-β. In spite of the potent suppressor capacity displayed by this CD62L− T reg cell population, the natural CD62L+ T reg cells remained defective in infliximab-treated patients. These results suggest that anti–TNF-α therapy in RA patients generates a newly differentiated population of T reg cells, which compensates for the defective natural T reg cells. Therefore, manipulation of a proinflammatory environment could represent a therapeutic strategy for the induction of T reg cells and the restoration of tolerance.
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Cites
Control of Regulatory T Cell Development by the Transcription Factor Foxp3
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Transforming growth factor-β induces development of the TH17 lineage
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CD127 expression inversely correlates with FoxP3 and suppressive function of human CD4+ T reg cells
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Th17: An Effector CD4 T Cell Lineage with Regulatory T Cell Ties
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Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines
Rea, I. M., Gibson, D. S., McGilligan, V., McNerlan, S. E., Alexander, H. D., & Ross, O. A. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00586 · Cited by 1,267
Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis
Komatsu, N., Okamoto, K., Sawa, S., Nakashima, T., Oh-hora, M., Kodama, T., Tanaka, S., Bluestone, J. A., & Takayanagi, H. (2014) · Nature Medicine · doi:10.1038/nm.3432 · Cited by 1,153
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Brzustewicz, E., & Bryl, E. (2015) · Cytokine · doi:10.1016/j.cyto.2015.08.260 · Cited by 196
Li, J.-Y., Duan, X.-F., Wang, L.-P., Xu, Y.-J., Huang, L., Zhang, T.-F., Liu, J.-Y., Li, F., Zhang, Z., Yue, D.-L., et al. (2014) · Journal of Immunology Research · doi:10.1155/2014/286170 · Cited by 157
T Regulatory Cells in Bone Remodelling
Bozec, A., & Zaiss, M. M. (2017) · Current Osteoporosis Reports · doi:10.1007/s11914-017-0356-1 · Cited by 110
Afroz, S., Giddaluru, J., Vishwakarma, S., Naz, S., Khan, A. A., & Khan, N. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00074 · Cited by 50
Metadata
- Authors
- Nadkarni, S., Mauri, C., & Ehrenstein, M. R.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2007-01-02
- Volume
- 204
- Issue
- 1
- Pages
- 33-39
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2097057955
- Cited by
- 507
- References
- 6
- FWCI
- 17.33
- Type
- journal article
- Language
- en
- Open access
- bronze
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