B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.

<h4>Background</h4>Dendritic cells (DC) can act tolerogenic at a semi-mature stage by induction of protective CD4(+) T cell and NKT cell responses.<h4>Methodology/principal findings</h4>Here we studied the role of the co-inhibitory molecule B7-H1 (PD-L1, CD274) on semi-mature...

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Autores principales: Carolin Brandl, Sonja Ortler, Thomas Herrmann, Susanna Cardell, Manfred B Lutz, Heinz Wiendl
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Publicado: Public Library of Science (PLoS) 2010
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spelling oai:doaj.org-article:b31f1ec16bec437daa228ad4988f72132021-12-02T20:21:25ZB7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.1932-620310.1371/journal.pone.0010800https://doaj.org/article/b31f1ec16bec437daa228ad4988f72132010-05-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20520738/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Dendritic cells (DC) can act tolerogenic at a semi-mature stage by induction of protective CD4(+) T cell and NKT cell responses.<h4>Methodology/principal findings</h4>Here we studied the role of the co-inhibitory molecule B7-H1 (PD-L1, CD274) on semi-mature DC that were generated from bone marrow (BM) cells of B7-H1(-/-) mice and applied to the model of Experimental Autoimmune Encephalomyelitis (EAE). Injections of B7-H1-deficient DC showed increased EAE protection as compared to wild type (WT)-DC. Injections of B7-H1(-/-) TNF-DC induced higher release of peptide-specific IL-10 and IL-13 after restimulation in vitro together with elevated serum cytokines IL-4 and IL-13 produced by NKT cells, and reduced IL-17 and IFN-gamma production in the CNS. Experiments in CD1d(-/-) and Jalpha281(-/-) mice as well as with type I and II NKT cell lines indicated that only type II NKT cells but not type I NKT cells (invariant NKT cells) could be stimulated by an endogenous CD1d-ligand on DC and were responsible for the increased serum cytokine production in the absence of B7-H1.<h4>Conclusions/significance</h4>Together, our data indicate that BM-DC express an endogenous CD1d ligand and B7-H1 to ihibit type II but not type I NKT cells. In the absence of B7-H1 on these DC their tolerogenic potential to stimulate tolerogenic CD4(+) and NKT cell responses is enhanced.Carolin BrandlSonja OrtlerThomas HerrmannSusanna CardellManfred B LutzHeinz WiendlPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 5, p e10800 (2010)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Carolin Brandl
Sonja Ortler
Thomas Herrmann
Susanna Cardell
Manfred B Lutz
Heinz Wiendl
B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.
description <h4>Background</h4>Dendritic cells (DC) can act tolerogenic at a semi-mature stage by induction of protective CD4(+) T cell and NKT cell responses.<h4>Methodology/principal findings</h4>Here we studied the role of the co-inhibitory molecule B7-H1 (PD-L1, CD274) on semi-mature DC that were generated from bone marrow (BM) cells of B7-H1(-/-) mice and applied to the model of Experimental Autoimmune Encephalomyelitis (EAE). Injections of B7-H1-deficient DC showed increased EAE protection as compared to wild type (WT)-DC. Injections of B7-H1(-/-) TNF-DC induced higher release of peptide-specific IL-10 and IL-13 after restimulation in vitro together with elevated serum cytokines IL-4 and IL-13 produced by NKT cells, and reduced IL-17 and IFN-gamma production in the CNS. Experiments in CD1d(-/-) and Jalpha281(-/-) mice as well as with type I and II NKT cell lines indicated that only type II NKT cells but not type I NKT cells (invariant NKT cells) could be stimulated by an endogenous CD1d-ligand on DC and were responsible for the increased serum cytokine production in the absence of B7-H1.<h4>Conclusions/significance</h4>Together, our data indicate that BM-DC express an endogenous CD1d ligand and B7-H1 to ihibit type II but not type I NKT cells. In the absence of B7-H1 on these DC their tolerogenic potential to stimulate tolerogenic CD4(+) and NKT cell responses is enhanced.
format article
author Carolin Brandl
Sonja Ortler
Thomas Herrmann
Susanna Cardell
Manfred B Lutz
Heinz Wiendl
author_facet Carolin Brandl
Sonja Ortler
Thomas Herrmann
Susanna Cardell
Manfred B Lutz
Heinz Wiendl
author_sort Carolin Brandl
title B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.
title_short B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.
title_full B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.
title_fullStr B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.
title_full_unstemmed B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells.
title_sort b7-h1-deficiency enhances the potential of tolerogenic dendritic cells by activating cd1d-restricted type ii nkt cells.
publisher Public Library of Science (PLoS)
publishDate 2010
url https://doaj.org/article/b31f1ec16bec437daa228ad4988f7213
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