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dc.contributor.authorKnothe, S
dc.contributor.authorMutschler, V
dc.contributor.authorRochlitzer, S
dc.contributor.authorWinkler, C
dc.contributor.authorEbensen, T
dc.contributor.authorGuzman, C A
dc.contributor.authorHohlfeld, J
dc.contributor.authorBraun, A
dc.contributor.authorMuller, M
dc.date.accessioned2011-07-01T13:53:14Z
dc.date.available2011-07-01T13:53:14Z
dc.date.issued2011-06-06
dc.identifier.citationThe NKT cell ligand αgalactosylceramide suppresses allergic airway inflammation by induction of a Th1 response. 2011, 29 (25):4249-55 Vaccineen
dc.identifier.issn1873-2518
dc.identifier.pmid21463684
dc.identifier.doi10.1016/j.vaccine.2011.03.068
dc.identifier.urihttp://hdl.handle.net/10033/135059
dc.description.abstractOne experimental approach for the treatment of allergic reactions is the stimulation of immunoregulatory NKT cells with the synthetic glycolipid αgalactosylceramide. For a first evaluation of the immunomodulatory potential of αGalCerMPEG a human in vitro allergy model was exploited. Acting as an adjuvant, the glycolipid induced an enhanced Th1-biased allergen-specific immune response of autologous lymphocytes. In a mouse model of allergic airway inflammation, αGalCerMPEG-activated NKT cells promoted a cytokine environment in the spleen, leading to priming of Th1 cells. The shift towards a Th1-dominated allergen-specific immune response thus might mediate the abrogation of allergic airway inflammation and thereby might provide a valid option for therapeutic intervention.
dc.language.isoenen
dc.titleThe NKT cell ligand αgalactosylceramide suppresses allergic airway inflammation by induction of a Th1 response.en
dc.typeArticleen
dc.contributor.departmentFraunhofer Institute for Toxicology and Experimental Medicine, Department of Immunology, Allergology and Immunotoxicology, Nikolai-Fuchs-Str. 1, 30625 Hannover, Germany.en
dc.identifier.journalVaccineen
refterms.dateFOA2018-06-13T07:24:30Z
html.description.abstractOne experimental approach for the treatment of allergic reactions is the stimulation of immunoregulatory NKT cells with the synthetic glycolipid αgalactosylceramide. For a first evaluation of the immunomodulatory potential of αGalCerMPEG a human in vitro allergy model was exploited. Acting as an adjuvant, the glycolipid induced an enhanced Th1-biased allergen-specific immune response of autologous lymphocytes. In a mouse model of allergic airway inflammation, αGalCerMPEG-activated NKT cells promoted a cytokine environment in the spleen, leading to priming of Th1 cells. The shift towards a Th1-dominated allergen-specific immune response thus might mediate the abrogation of allergic airway inflammation and thereby might provide a valid option for therapeutic intervention.


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