The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Prostaglandin E2 synergistically with interleukin-23 favors human Th17 expansion
Open accessAbstract
Microenvironment molecular cues direct T helper (Th) cell differentiation; however, Th17 fate determination is still imprecisely understood in humans. To assess the role of prostaglandin E2 (PGE2) in Th expansion, we activated peripheral blood mononuclear cells by CD3 cross-linking. In the presence of exogenous PGE2, peripheral blood mononuclear cells produced higher interleukin-17 (IL-17), C-C chemokine ligand 20 (CCL20)/macrophage inflammatory protein 3α (MIP-3α), CXC chemokine ligand 8 (CXCL8)/IL-8, and lower interferon-γ and IL-22 levels than in control cultures. Exogenous PGE2 and IL-23 synergized in inducing IL-17, whereas indomethacin and IL-23 blockade drastically reduced IL-17 but not interferon-γ production. Furthermore, IL-1 but not tumor necrosis factor was absolutely required for IL-17 production. PGE2 doubled the frequency of CD4+ T cells producing IL-17 and within the CD4+ subset enhanced C-C chemokine receptor 6 (CCR6) and CCR4 while decreasing CXC chemokine receptor 3 (CXCR3) expression. Furthermore, in CD4+ T-cell lines, the production of IL-17 segregated with the CCR6+ subset. In the presence of CCR6+ compared with CXCR3+ Th cells, monocytes/macrophages produced much higher levels of matrix metalloproteinase-1, -3, and -9 but similar levels of CXCL10 and IL-1β. These results identify PGE2 and IL-23 as participating in the expansion of CD4+ T cells endowed with high IL-17 production capacity, which in turn favors monocyte production of mediators important for host defense and tissue destruction.
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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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Phenotypic and functional features of human Th17 cells
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Dinarello, C. A. (2011) · Blood · doi:10.1182/blood-2010-07-273417 · Cited by 2,248
Yao, C., Sakata, D., Esaki, Y., Li, Y., Matsuoka, T., Kuroiwa, K., Sugimoto, Y., & Narumiya, S. (2009) · Nature Medicine · doi:10.1038/nm.1968 · Cited by 566
Prostaglandin E2-induced inflammation: Relevance of prostaglandin E receptors
Kawahara, K., Hohjoh, H., Inazumi, T., Tsuchiya, S., & Sugimoto, Y. (2015) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2014.07.008 · Cited by 488
Protumor vs Antitumor Functions of IL-17
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Metadata
- Authors
- Chizzolini, C., Chicheportiche, R., Alvarez, M., de Rham, C., Roux-Lombard, P., Ferrari-Lacraz, S., & Dayer, J.-M.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2008-11-01
- Volume
- 112
- Issue
- 9
- Pages
- 3696-3703
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2005536703
- Cited by
- 235
- References
- 14
- FWCI
- 9.57
- Type
- journal article
- Language
- en
- Open access
- green
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- Chizzolini, C., Chicheportiche, R., Alvarez, M., de Rham, C., Roux-Lombard, P., Ferrari-Lacraz, S., & Dayer, J.-M. (2008). Prostaglandin E2 synergistically with interleukin-23 favors human Th17 expansion. Blood. https://doi.org/10.1182/blood-2008-05-155408
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