Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7274
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dc.contributor.authorRiegel, Kristina-
dc.contributor.authorYurugi, Hajime-
dc.contributor.authorSchlöder, Janine-
dc.contributor.authorJonuleit, Helmut-
dc.contributor.authorKaulich, Manuel-
dc.contributor.authorKirschner, Friederike-
dc.contributor.authorArnold-Schild, Danielle-
dc.contributor.authorTenzer, Stefan-
dc.contributor.authorSchild, Hansjörg-
dc.contributor.authorRajalingam, Krishnaraj-
dc.date.accessioned2022-07-01T08:58:15Z-
dc.date.available2022-07-01T08:58:15Z-
dc.date.issued2021-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7288-
dc.description.abstractTumors exhibit a variety of strategies to dampen antitumor immune responses. With an aim to identify factors that are secreted from tumor cells, we performed an unbiased mass spectrometry-based secretome analysis in lung cancer cells. Interleukin-6 (IL-6) has been identified as a prominent factor secreted by tumor cells and cancer-associated fibroblasts isolated from cancer patients. Incubation of dendritic cell (DC) cultures with tumor cell supernatants inhibited the production of IL-12p70 in DCs but not the surface expression of other activation markers which is reversed by treatment with IL-6 antibody. Defects in IL-12p70 production in the DCs inhibited the differentiation of Th1 but not Th2 and Th17 cells from naïve CD4+ T cells. We also demonstrate that the classical mitogen-activated protein kinase, ERK5/MAPK7, is required for IL-6 production in tumor cells. Inhibition of ERK5 activity or depletion of ERK5 prevented IL-6 production in tumor cells, which could be exploited for enhancing antitumor immune responses.en_GB
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleERK5 modulates IL-6 secretion and contributes to tumor-induced immune suppressionen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7274-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleCell death & diseasede
jgu.journal.volume12de
jgu.pages.alternative969de
jgu.publisher.year2021-
jgu.publisher.nameNature Publishing Groupde
jgu.publisher.placeLondon u.a.de
jgu.publisher.issn2041-4889de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1038/s41419-021-04257-8de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:JGU-Publikationen

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