Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-8112
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dc.contributor.authorGladigau, Gerd-
dc.contributor.authorHaselmayer, Philipp-
dc.contributor.authorScharrer, Inge-
dc.contributor.authorMunder, Markus-
dc.contributor.authorPrinz, Nadine-
dc.contributor.authorLackner, Karl J.-
dc.contributor.authorSchild, Hansjörg-
dc.contributor.authorStein, Pamela-
dc.contributor.authorRadsak, Markus-
dc.date.accessioned2022-10-20T07:55:46Z-
dc.date.available2022-10-20T07:55:46Z-
dc.date.issued2012-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/8127-
dc.description.abstractThe anti-phospholipid syndrome (APS) is characterized by recurrent thrombosis and occurrence of anti-phospholipid antibodies (aPL). aPL are necessary, but not sufficient for the clinical manifestations of APS. Growing evidence suggests a role of innate immune cells, in particular polymorphonuclear neutrophils (PMN) and Toll-like receptors (TLR) to be additionally involved. aPL activate endothelial cells and monocytes through a TLR4-dependent signalling pathway. Whether this is also relevant for PMN in a similar way is currently not known. To address this issue, we used purified PMN from healthy donors and stimulated them in the presence or absence of human monoclonal aPL and the TLR4 agonist LPS monitoring neutrophil effector functions, namely the oxidative burst, phagocytosis, L-Selectin shedding and IL-8 production. aPL alone were only able to induce minor activation of PMN effector functions at high concentrations. However, in the additional presence of LPS the activation threshold was markedly lower indicating a synergistic activation pathway of aPL and TLR in PMN. In summary, our results indicate that PMN effector functions are directly activated by aPL and boosted by the additional presence of microbial products. This highlights a role for PMN as important innate immune effector cells that contribute to the pathophysiology of APS.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleA role for Toll-like receptor mediated signals in neutrophils in the pathogenesis of the anti-phospholipid syndromeen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-8112-
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.titlePLoS onede
jgu.journal.volume7de
jgu.journal.issue7de
jgu.pages.start1de
jgu.pages.end9de
jgu.pages.alternativee42176de
jgu.publisher.year2012-
jgu.publisher.namePLoSde
jgu.publisher.placeLawrence, Kan.de
jgu.publisher.urihttp://dx.doi.org/10.1371/journal.pone.0042176de
jgu.publisher.issn1932-6203de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2013-07-02T08:27:10Z-
opus.subject.dfgcode04-205-
opus.organisation.stringFB 04: Medizin: Institut für Klinische Chemie und Laboratoriumsmedizinde_DE
opus.organisation.stringFB 04: Medizin: III. Medizinische Klinik und Poliklinikde_DE
opus.organisation.stringFB 04: Medizin: Institut für Immunologiede_DE
opus.identifier.opusid22549-
opus.institute.number0428-
opus.institute.number0427-
opus.institute.number0412-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedScharrer, Inge-
opus.affiliatedLackner, Karl J.-
opus.affiliatedSchild, Hansjörg-
opus.affiliatedRadsak, Markus-
jgu.publisher.doi10.1371/journal.pone.0042176de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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