The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Essentials of Th17 cell commitment and plasticity
Open accessAbstract
CD4+ T helper (Th) cells exist in a variety of epigenetic states that determine their function, phenotype, and capacity for persistence. These polarization states include Th1, Th2, Th17, and Foxp3+ T regulatory cells, as well as the more recently described T follicular helper, Th9, and Th22 cells. Th17 cells express the master transcriptional regulator retinoic acid–related orphan receptor γ thymus and produce canonical interleukin (IL)-17A and IL-17F cytokines. Th17 cells display a great degree of context-dependent plasticity, as they are capable of acquiring functional characteristics of Th1 cells. This late plasticity may contribute to the protection against microbes, plays a role in the development of autoimmunity, and is necessary for antitumor activity of Th17 cells in adoptive cell transfer therapy models. Moreover, plasticity of this subset is associated with higher in vivo survival and self-renewal capacity and less senescence than Th1 polarized cells, which have less plasticity and more phenotypic stability. New findings indicate that subset polarization of CD4+ T cells not only induces characteristic patterns of surface markers and cytokine production but also has a maturational aspect that affects a cell’s ability to survive, respond to secondary stimulation, and form long-term immune memory.
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Citations
Cites
Control of Regulatory T Cell Development by the Transcription Factor Foxp3
Hori, S., Nomura, T., & Sakaguchi, S. (2003) · Science · doi:10.1126/science.1079490 · Cited by 8,187 · cited 1×
“The discovery of FoxP3-expressing regulatory CD4(1) T cells (Treg) that restrained immune responses complement these early views of Th differentiation.(26) However, not all CD4(1) T-cell activity could easily be classified as either type 1 or type 2.”
BackgroundIvanov, I. I., McKenzie, B. S., Zhou, L., Tadokoro, C. E., Lepelley, A., Lafaille, J. J., Cua, D. J., & Littman, D. R. (2006) · Cell · doi:10.1016/j.cell.2006.07.035 · Cited by 5,145
Korn, T., Bettelli, E., Oukka, M., & Kuchroo, V. K. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132710 · Cited by 4,873
Harrington, L. E., Hatton, R. D., Mangan, P. R., Turner, H., Murphy, T. L., Murphy, K. M., & Weaver, C. T. (2005) · Nature Immunology · doi:10.1038/ni1254 · Cited by 4,742
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
Park, H., Li, Z., Yang, X. O., Chang, S. H., Nurieva, R., Wang, Y.-H., Wang, Y., Hood, L., Zhu, Z., Tian, Q., et al. (2005) · Nature Immunology · doi:10.1038/ni1261 · Cited by 4,265
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
Veldhoen, M., Hocking, R. J., Atkins, C. J., Locksley, R. M., & Stockinger, B. (2006) · Immunity · doi:10.1016/j.immuni.2006.01.001 · Cited by 3,605 · cited 1×
“Thus, at low concentrations, TGF-b1 contributes indirectly to the initial development of Th17 responses but is not critical to the inflammatory milieu that drives type 17 responses.(62) At high concentrations, TGF-b signaling inhibits IL-23R expression and converts naı̈ve Th cells into induced FoxP3(1) regulatory cell…”
BackgroundImmunological and inflammatory functions of the interleukin-1 family
Dinarello, C. A. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132612 · Cited by 3,466
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
Cua, D. J., Sherlock, J., Chen, Y., Murphy, C. A., Joyce, B., Seymour, B., Lucian, L., To, W., Kwan, S., Churakova, T., et al. (2003) · Nature · doi:10.1038/nature01355 · Cited by 2,906
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
When worlds collide: Th17 and Treg cells in cancer and autoimmunity
Knochelmann, H. M., Dwyer, C. J., Bailey, S. R., Amaya, S. M., Elston, D. M., Mazza-McCrann, J. M., & Paulos, C. M. (2018) · Cellular & Molecular Immunology · doi:10.1038/s41423-018-0004-4 · Cited by 535
Basic biology and role of interleukin‐17 in immunity and inflammation
Zenobia, C., & Hajishengallis, G. (2015) · Periodontology 2000 · doi:10.1111/prd.12083 · Cited by 470
Alizadeh, D., Trad, M., Hanke, N. T., Larmonier, C. B., Janikashvili, N., Bonnotte, B., Katsanis, E., & Larmonier, N. (2014) · Cancer Research · doi:10.1158/0008-5472.can-13-1545 · Cited by 416
Clonal expansion of genome-intact HIV-1 in functionally polarized Th1 CD4+ T cells
Lee, G. Q., Orlova-Fink, N., Einkauf, K., Chowdhury, F. Z., Sun, X., Harrington, S., Kuo, H.-H., Hua, S., Chen, H.-R., Ouyang, Z., et al. (2017) · Journal of Clinical Investigation · doi:10.1172/jci93289 · Cited by 292
Metadata
- Authors
- Muranski, P., & Restifo, N. P.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2013-03-28
- Volume
- 121
- Issue
- 13
- Pages
- 2402-2414
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2070769098
- Cited by
- 383
- References
- 42
- FWCI
- 22.97
- Type
- journal article
- Language
- en
- Open access
- bronze
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