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Article: IL-7 engages multiple mechanisms to overcome chronic viral infection and limit organ pathology

TitleIL-7 engages multiple mechanisms to overcome chronic viral infection and limit organ pathology
Authors
Issue Date2011
Citation
Cell, 2011, v. 144, n. 4, p. 601-613 How to Cite?
AbstractUnderstanding the factors that impede immune responses to persistent viruses is essential in designing therapies for HIV infection. Mice infected with LCMV clone-13 have persistent high-level viremia and a dysfunctional immune response. Interleukin-7, a cytokine that is critical for immune development and homeostasis, was used here to promote immunity toward clone-13, enabling elucidation of the inhibitory pathways underlying impaired antiviral immune response. Mechanistically, IL-7 downregulated a critical repressor of cytokine signaling, Socs3, resulting in amplified cytokine production, increased T cell effector function and numbers, and viral clearance. IL-7 enhanced thymic output to expand the naive T cell pool, including T cells that were not LCMV specific. Additionally, IL-7 promoted production of cytoprotective IL-22 that abrogated liver pathology. The IL-7-mediated effects were dependent on endogenous IL-6. These attributes of IL-7 have profound implications for its use as a therapeutic in the treatment of chronic viral diseases. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/292018
ISSN
2023 Impact Factor: 45.5
2023 SCImago Journal Rankings: 24.342
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPellegrini, Marc-
dc.contributor.authorCalzascia, Thomas-
dc.contributor.authorToe, Jesse G.-
dc.contributor.authorPreston, Simon P.-
dc.contributor.authorLin, Amy E.-
dc.contributor.authorElford, Alisha R.-
dc.contributor.authorShahinian, Arda-
dc.contributor.authorLang, Philipp A.-
dc.contributor.authorLang, Karl S.-
dc.contributor.authorMorre, Michel-
dc.contributor.authorAssouline, Brigitte-
dc.contributor.authorLahl, Katharina-
dc.contributor.authorSparwasser, Tim-
dc.contributor.authorTedder, Thomas F.-
dc.contributor.authorPaik, Ji Hye-
dc.contributor.authorDePinho, Ronald A.-
dc.contributor.authorBasta, Sameh-
dc.contributor.authorOhashi, Pamela S.-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:55:36Z-
dc.date.available2020-11-17T14:55:36Z-
dc.date.issued2011-
dc.identifier.citationCell, 2011, v. 144, n. 4, p. 601-613-
dc.identifier.issn0092-8674-
dc.identifier.urihttp://hdl.handle.net/10722/292018-
dc.description.abstractUnderstanding the factors that impede immune responses to persistent viruses is essential in designing therapies for HIV infection. Mice infected with LCMV clone-13 have persistent high-level viremia and a dysfunctional immune response. Interleukin-7, a cytokine that is critical for immune development and homeostasis, was used here to promote immunity toward clone-13, enabling elucidation of the inhibitory pathways underlying impaired antiviral immune response. Mechanistically, IL-7 downregulated a critical repressor of cytokine signaling, Socs3, resulting in amplified cytokine production, increased T cell effector function and numbers, and viral clearance. IL-7 enhanced thymic output to expand the naive T cell pool, including T cells that were not LCMV specific. Additionally, IL-7 promoted production of cytoprotective IL-22 that abrogated liver pathology. The IL-7-mediated effects were dependent on endogenous IL-6. These attributes of IL-7 have profound implications for its use as a therapeutic in the treatment of chronic viral diseases. © 2011 Elsevier Inc.-
dc.languageeng-
dc.relation.ispartofCell-
dc.titleIL-7 engages multiple mechanisms to overcome chronic viral infection and limit organ pathology-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.cell.2011.01.011-
dc.identifier.pmid21295337-
dc.identifier.scopuseid_2-s2.0-79951713941-
dc.identifier.volume144-
dc.identifier.issue4-
dc.identifier.spage601-
dc.identifier.epage613-
dc.identifier.isiWOS:000287473100014-
dc.identifier.f10008506956-
dc.identifier.issnl0092-8674-

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