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- Publisher Website: 10.1016/S1074-7613(03)00300-5
- Scopus: eid_2-s2.0-0345570521
- PMID: 14614852
- WOS: WOS:000186672200005
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Article: The IL-27R (WSX-1) is required to suppress T cell hyperactivity during infection
Title | The IL-27R (WSX-1) is required to suppress T cell hyperactivity during infection |
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Authors | |
Issue Date | 2003 |
Citation | Immunity, 2003, v. 19, n. 5, p. 645-655 How to Cite? |
Abstract | Although recent studies have described IL-27 and its receptor, WSX-1, as promoters of Th1 differentiation in naive CD4+ T cells, the data presented here indicate that signaling through this receptor is involved in limiting the intensity and duration of T cell activity. When WSX-1-deficient mice are infected with the intracellular pathogen Toxoplasma gondii, they establish protective T cell responses, characterized by production of inflammatory cytokines and control of parasite replication. However, infected WSX-1-/- mice are unable to downregulate these protective responses, and develop a lethal, T cell-mediated inflammatory disease. This pathology was characterized by the excessive production of IFN-γ, persistence of highly activated T cells, and enhanced T cell proliferation in vivo. Together, these findings demonstrate that WSX-1 is not required for the generation of IFN-γ-mediated immunity to this parasitic infection and identify a novel function for this receptor as a potent antagonist of T cell-mediated, immune hyperactivity. |
Persistent Identifier | http://hdl.handle.net/10722/291670 |
ISSN | 2023 Impact Factor: 25.5 2023 SCImago Journal Rankings: 13.578 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Villarino, Alejandro | - |
dc.contributor.author | Hibbert, Linda | - |
dc.contributor.author | Lieberman, Linda | - |
dc.contributor.author | Wilson, Emma | - |
dc.contributor.author | Mak, Tak | - |
dc.contributor.author | Yoshida, Hiroki | - |
dc.contributor.author | Kastelein, Robert A. | - |
dc.contributor.author | Saris, Christiaan | - |
dc.contributor.author | Hunter, Christopher A. | - |
dc.date.accessioned | 2020-11-17T14:54:52Z | - |
dc.date.available | 2020-11-17T14:54:52Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Immunity, 2003, v. 19, n. 5, p. 645-655 | - |
dc.identifier.issn | 1074-7613 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291670 | - |
dc.description.abstract | Although recent studies have described IL-27 and its receptor, WSX-1, as promoters of Th1 differentiation in naive CD4+ T cells, the data presented here indicate that signaling through this receptor is involved in limiting the intensity and duration of T cell activity. When WSX-1-deficient mice are infected with the intracellular pathogen Toxoplasma gondii, they establish protective T cell responses, characterized by production of inflammatory cytokines and control of parasite replication. However, infected WSX-1-/- mice are unable to downregulate these protective responses, and develop a lethal, T cell-mediated inflammatory disease. This pathology was characterized by the excessive production of IFN-γ, persistence of highly activated T cells, and enhanced T cell proliferation in vivo. Together, these findings demonstrate that WSX-1 is not required for the generation of IFN-γ-mediated immunity to this parasitic infection and identify a novel function for this receptor as a potent antagonist of T cell-mediated, immune hyperactivity. | - |
dc.language | eng | - |
dc.relation.ispartof | Immunity | - |
dc.title | The IL-27R (WSX-1) is required to suppress T cell hyperactivity during infection | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1016/S1074-7613(03)00300-5 | - |
dc.identifier.pmid | 14614852 | - |
dc.identifier.scopus | eid_2-s2.0-0345570521 | - |
dc.identifier.volume | 19 | - |
dc.identifier.issue | 5 | - |
dc.identifier.spage | 645 | - |
dc.identifier.epage | 655 | - |
dc.identifier.isi | WOS:000186672200005 | - |
dc.identifier.f1000 | 1016282 | - |
dc.identifier.issnl | 1074-7613 | - |