Lühder, Fred

[["dc.bibliographiccitation.firstpage","1644"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","1655"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Froehlich, Monika"],["dc.contributor.author","Gogishvili, Tea"],["dc.contributor.author","Langenhorst, Daniela"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Huenig, Thomas"],["dc.date.accessioned","2018-11-07T10:11:59Z"],["dc.date.available","2018-11-07T10:11:59Z"],["dc.date.issued","2016"],["dc.description.abstract","The role of CD28-mediated costimulation in secondary CD8(+) T-cell responses remains controversial. Here, we have used two tools - blocking mouse anti-mouse CD28-specific antibodies and inducible CD28-deleting mice - to obtain definitive answers in mice infected with ovalbumin-secreting Listeria monocytogenes. We report that both blockade and global deletion of CD28 reveal its requirement for full clonal expansion and effector functions such as degranulation and IFN-gamma production during the secondary immune response. In contrast, cell-intrinsic deletion of CD28 in transferred TCR-transgenic CD8(+) T cells before primary infection leads to impaired clonal expansion but an increase in cells able to express effector functions in both primary and secondary responses. We suggest that the proliferation-impaired CD8(+) T cells respond to CD28-dependent help from their environment by enhanced functional differentiation. Finally, we report that cell-intrinsic deletion of CD28 after the peak of the primary response does not affect the establishment, maintenance, or recall of long-term memory. Thus, if given sufficient time, the progeny of primed CD8(+) T cells adapt to the absence of this costimulator."],["dc.identifier.doi","10.1002/eji.201546232"],["dc.identifier.isi","000380752600013"],["dc.identifier.pmid","27122236"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40149"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.title","Interrupting CD28 costimulation before antigen rechallenge affects CD8(+) T-cell expansion and effector functions during secondary response in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1394"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Allergy and Clinical Immunology"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Gogishvili, Tea"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Kirstein, Frank"],["dc.contributor.author","Nieuwenhuizen, Natalie E."],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Beer-Hammer, Sandra"],["dc.contributor.author","Pfeffer, Klaus"],["dc.contributor.author","Reuter, Sebastian"],["dc.contributor.author","Taube, Christian"],["dc.contributor.author","Brombacher, Frank"],["dc.contributor.author","Huenig, Thomas"],["dc.date.accessioned","2018-11-07T09:02:49Z"],["dc.date.available","2018-11-07T09:02:49Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: Allergic asthma is a T(H)2-promoted hyperreactivity with an immediate, IgE, and mast cell-dependent response followed by eosinophil-dominated inflammation and airway obstruction. Objective: Because costimulation by CD28 is essential for T(H)2 but not T(H)1 responses, we investigated the effect of selective interference with this pathway in mice using the models of ovalbumin and house dust mite-induced airway inflammation. Methods: To study the role of CD28 in the effector phase of allergic airway inflammation, we developed an inducibly CD28-deleting mouse strain or alternatively used a CD28 ligand-binding site-specific mouse anti-mouse mAb blocking CD28 engagement. Results: We show that even after systemic sensitization to the allergen, interruption of CD28-mediated costimulation is highly effective in preventing airway inflammation during challenge. In addition to improving airway resistance and histopathologic presentation and reducing inflammatory infiltrates, antibody treatment during allergen challenge resulted in a marked relative increase in regulatory T-cell numbers among the CD4 T-cell subset of the challenged lung. Conclusion: Selective interference with CD28-mediated costimulation during allergen exposure might be an attractive therapeutic concept for allergic asthma. (J Allergy Clin Immunol 2012;130:1394-403.)"],["dc.identifier.doi","10.1016/j.jaci.2012.08.049"],["dc.identifier.isi","000311641100021"],["dc.identifier.pmid","23102920"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24769"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mosby-elsevier"],["dc.relation.issn","0091-6749"],["dc.title","Interruption of CD28-mediated costimulation during allergen challenge protects mice from allergic airway disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Huenig, Thomas"],["dc.contributor.author","Beyersdorf, Niklas"],["dc.contributor.author","Dennehy, Kevin M."],["dc.contributor.author","Lin, C."],["dc.contributor.author","Ellas, F."],["dc.contributor.author","Kerkau, Thomas"],["dc.contributor.author","Gaupp, S."],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Na, S."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T09:33:24Z"],["dc.date.available","2018-11-07T09:33:24Z"],["dc.date.issued","2006"],["dc.format.extent","27"],["dc.identifier.isi","000249372500079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31958"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","B M J Publishing Group"],["dc.publisher.place","London"],["dc.relation.conference","Annual European Congress of Rheumatology (EULAR 2006)"],["dc.relation.eventlocation","Amsterdam, NETHERLANDS"],["dc.relation.issn","0003-4967"],["dc.title","CD28-stimulated expansion of regulatory T-cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","178"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Na, Shin-Young"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Huenig, Thomas"],["dc.date.accessioned","2018-11-07T09:20:44Z"],["dc.date.available","2018-11-07T09:20:44Z"],["dc.date.issued","2006"],["dc.format.extent","28"],["dc.identifier.isi","000241633100063"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28947"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Nagoya, JAPAN"],["dc.relation.issn","0165-5728"],["dc.title","Recruitment of regulatory T-cells to treat EAE"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","188"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","193"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Gogishvili, Tea"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Beer-Hammer, Sandra"],["dc.contributor.author","Pfeffer, Klaus"],["dc.contributor.author","Huenig, Thomas"],["dc.date.accessioned","2018-11-07T09:30:36Z"],["dc.date.available","2018-11-07T09:30:36Z"],["dc.date.issued","2013"],["dc.description.abstract","While the requirement for CD28 and its ligands for the generation and function of natural (n)Treg cells is well established, it has not been possible yet to investigate cell-intrinsic effects after interrupted CD28 expression. Here, we demonstrate a selective loss of Treg cells after disruption of the CD28 gene. The decline in Treg-cell number was accompanied by reduced homeostatic proliferation, probably due to lack of costimulation during self-antigen recognition, and by impaired Treg-cell function including downregulation of CTLA-4. The decline in Treg-cell number was unaffected by thymectomy or by the presence of CD28 expressing T cells within the same animal, indicating that impairment of peripheral homeostasis and function of nTreg cells by CD28 deletion is cell-intrinsic. In contrast, downregulation of CD25, the a chain of the IL-2R, did not occur in the presence of WT T cells, indicating that its expression does not depend on CD28 signals in cis."],["dc.identifier.doi","10.1002/eji.201242824"],["dc.identifier.isi","000313883200026"],["dc.identifier.pmid","23065717"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31340"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.title","Cell-intrinsic and -extrinsic control of Treg-cell homeostasis and function revealed by induced CD28 deletion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]