Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-6185
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dc.contributor.authorBednarczyk, Monika-
dc.contributor.authorMedina-Montano, Carolina-
dc.contributor.authorFittler, Frederic Julien-
dc.contributor.authorStege, Henner-
dc.contributor.authorRoskamp, Meike-
dc.contributor.authorKuske, Michael-
dc.contributor.authorLanger, Christian-
dc.contributor.authorVahldieck, Marco-
dc.contributor.authorMontermann, Evelyn-
dc.contributor.authorTubbe, Ingrid-
dc.contributor.authorRöhrig, Nadine-
dc.contributor.authorDzionek, Andrzej-
dc.contributor.authorGrabbe, Stephan-
dc.contributor.authorBros, Matthias-
dc.date.accessioned2021-07-09T10:02:55Z-
dc.date.available2021-07-09T10:02:55Z-
dc.date.issued2021-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/6194-
dc.description.abstractThe development of nanocarriers (NC) for biomedical applications has gained large interest due to their potential to co-deliver drugs in a cell-type-targeting manner. However, depending on their surface characteristics, NC accumulate serum factors, termed protein corona, which may affect their cellular binding. We have previously shown that NC coated with carbohydrates to enable biocompatibility triggered the lectin-dependent complement pathway, resulting in enhanced binding to B cells via complement receptor (CR)1/2. Here we show that such NC also engaged all types of splenic leukocytes known to express CR3 at a high rate when NC were pre-incubated with native mouse serum resulting in complement opsonization. By focusing on dendritic cells (DC) as an important antigen-presenting cell type, we show that CR3 was essential for binding/uptake of complement-opsonized NC, whereas CR4, which in mouse is specifically expressed by DC, played no role. Further, a minor B cell subpopulation (B-1), which is important for first-line pathogen responses, and co-expressed CR1/2 and CR3, in general, engaged NC to a much higher extent than normal B cells. Here, we identified CR-1/2 as necessary for binding of complement-opsonized NC, whereas CR3 was dispensable. Interestingly, the binding of complement-opsonized NC to both DC and B-1 cells affected the expression of activation markers. Our findings may have important implications for the design of nano-vaccines against infectious diseases, which codeliver pathogen-specific protein antigen and adjuvant, aimed to induce a broad adaptive cellular and humoral immune response by inducing cytotoxic T lymphocytes that kill infected cells and pathogen-neutralizing antibodies, respectively. Decoration of nano-vaccines either with carbohydrates to trigger complement activation in vivo or with active complement may result in concomitant targeting of DC and B cells and thereby may strongly enhance the extent of dual cellular/humoral immune responses.en_GB
dc.description.sponsorshipOpen Access-Publizieren Universität Mainz / Universitätsmedizin Mainzde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc540 Chemiede_DE
dc.subject.ddc540 Chemistry and allied sciencesen_GB
dc.subject.ddc570 Biowissenschaftende_DE
dc.subject.ddc570 Life sciencesen_GB
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleComplement-opsonized nano-carriers are bound by dendritic cells (DC) via complement receptor (CR)3, and by B cell subpopulations via CR-1/2, and affect the activation of DC and B-1 cellsen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-6185-
jgu.type.contenttypeScientific articlede
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.titleInternational journal of molecular sciencesde
jgu.journal.volume22de
jgu.journal.issue6de
jgu.pages.alternative2869de
jgu.publisher.year2021-
jgu.publisher.nameMolecular Diversity Preservation Internationalde
jgu.publisher.placeBaselde
jgu.publisher.urihttps://doi.org/10.3390/ijms22062869de
jgu.publisher.issn1422-0067de
jgu.publisher.issn1661-6596de
jgu.organisation.placeMainz-
jgu.subject.ddccode540de
jgu.subject.ddccode570de
jgu.subject.ddccode610de
jgu.publisher.doi10.3390/ijms22062869
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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