Refine
Has Fulltext
- yes (10)
Is part of the Bibliography
- yes (10)
Document Type
- Journal article (10)
Language
- English (10)
Keywords
- multiple sclerosis (2)
- B cells (1)
- C57BL/6 mice (1)
- CLN3 (1)
- Dendritische Zelle (1)
- EAE (1)
- GRAID (1)
- Guillain-Barre-Syndrome (1)
- IL-15 (1)
- K+ channel (1)
Institute
- Neurologische Klinik und Poliklinik (8)
- Medizinische Klinik und Poliklinik II (2)
- Institut für Anatomie und Zellbiologie (1)
- Institut für Klinische Biochemie und Pathobiochemie (1)
- Institut für Virologie und Immunbiologie (1)
- Klinik und Poliklinik für Psychiatrie, Psychosomatik und Psychotherapie (1)
- Rudolf-Virchow-Zentrum (1)
EU-Project number / Contract (GA) number
- 026155 (1)
Background: Dendritic cells (DC) can act tolerogenic at a semi-mature stage by induction of protective CD4+ T cell and NKT cell responses. Methodology/Principal Findings: Here we studied the role of the co-inhibitory molecule B7-H1 (PD-L1, CD274) on semimature DC that were generated from bone marrow (BM) cells of B7-H12/2 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-H12/2 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-c production in the CNS. Experiments in CD1d2/2 and Ja2812/2 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. Conclusions/Significance: 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.