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Article: Toso regulates differentiation and activation of inflammatory dendritic cells during persistence-prone virus infection

TitleToso regulates differentiation and activation of inflammatory dendritic cells during persistence-prone virus infection
Authors
Issue Date2015
Citation
Cell Death and Differentiation, 2015, v. 22, n. 1, p. 164-173 How to Cite?
AbstractDuring virus infection and autoimmune disease, inflammatory dendritic cells (iDCs) differentiate from blood monocytes and infiltrate infected tissue. Following acute infection with hepatotropic viruses, iDCs are essential for re-stimulating virus-specific CD8 + T cells and therefore contribute to virus control. Here we used the lymphocytic choriomeningitis virus (LCMV) model system to identify novel signals, which influence the recruitment and activation of iDCs in the liver. We observed that intrinsic expression of Toso (Faim3, FcμR) influenced the differentiation and activation of iDCs in vivo and DCs in vitro. Lack of iDCs in Toso-deficient (Toso -/-) mice reduced CD8 + T-cell function in the liver and resulted in virus persistence. Furthermore, Toso -/- DCs failed to induce autoimmune diabetes in the rat insulin promoter-glycoprotein (RIP-GP) autoimmune diabetes model. In conclusion, we found that Toso has an essential role in the differentiation and maturation of iDCs, a process that is required for the control of persistence-prone virus infection.
Persistent Identifierhttp://hdl.handle.net/10722/292878
ISSN
2023 Impact Factor: 13.7
2023 SCImago Journal Rankings: 4.102
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLang, P. A.-
dc.contributor.authorMeryk, A.-
dc.contributor.authorPandyra, A. A.-
dc.contributor.authorBrenner, D.-
dc.contributor.authorBrüstle, A.-
dc.contributor.authorXu, H. C.-
dc.contributor.authorMerches, K.-
dc.contributor.authorLang, F.-
dc.contributor.authorKhairnar, V.-
dc.contributor.authorSharma, P.-
dc.contributor.authorFunkner, P.-
dc.contributor.authorRecher, M.-
dc.contributor.authorShaabani, N.-
dc.contributor.authorDuncan, G. S.-
dc.contributor.authorDuhan, V.-
dc.contributor.authorHomey, B.-
dc.contributor.authorOhashi, P. S.-
dc.contributor.authorHäussinger, D.-
dc.contributor.authorKnolle, P. A.-
dc.contributor.authorHonke, N.-
dc.contributor.authorMak, T. W.-
dc.contributor.authorLang, K. S.-
dc.date.accessioned2020-11-17T14:57:24Z-
dc.date.available2020-11-17T14:57:24Z-
dc.date.issued2015-
dc.identifier.citationCell Death and Differentiation, 2015, v. 22, n. 1, p. 164-173-
dc.identifier.issn1350-9047-
dc.identifier.urihttp://hdl.handle.net/10722/292878-
dc.description.abstractDuring virus infection and autoimmune disease, inflammatory dendritic cells (iDCs) differentiate from blood monocytes and infiltrate infected tissue. Following acute infection with hepatotropic viruses, iDCs are essential for re-stimulating virus-specific CD8 + T cells and therefore contribute to virus control. Here we used the lymphocytic choriomeningitis virus (LCMV) model system to identify novel signals, which influence the recruitment and activation of iDCs in the liver. We observed that intrinsic expression of Toso (Faim3, FcμR) influenced the differentiation and activation of iDCs in vivo and DCs in vitro. Lack of iDCs in Toso-deficient (Toso -/-) mice reduced CD8 + T-cell function in the liver and resulted in virus persistence. Furthermore, Toso -/- DCs failed to induce autoimmune diabetes in the rat insulin promoter-glycoprotein (RIP-GP) autoimmune diabetes model. In conclusion, we found that Toso has an essential role in the differentiation and maturation of iDCs, a process that is required for the control of persistence-prone virus infection.-
dc.languageeng-
dc.relation.ispartofCell Death and Differentiation-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleToso regulates differentiation and activation of inflammatory dendritic cells during persistence-prone virus infection-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/cdd.2014.138-
dc.identifier.pmid25257173-
dc.identifier.pmcidPMC4262783-
dc.identifier.scopuseid_2-s2.0-84928479011-
dc.identifier.volume22-
dc.identifier.issue1-
dc.identifier.spage164-
dc.identifier.epage173-
dc.identifier.eissn1476-5403-
dc.identifier.isiWOS:000347841600017-
dc.identifier.issnl1350-9047-

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