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Constanze Voigtländer

Researcher at University of Erlangen-Nuremberg

Publications -  6
Citations -  961

Constanze Voigtländer is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Immune tolerance & Cytokine. The author has an hindex of 5, co-authored 6 publications receiving 932 citations.

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Journal ArticleDOI

Repetitive Injections of Dendritic Cells Matured with Tumor Necrosis Factor α Induce Antigen-specific Protection of Mice from Autoimmunity

TL;DR: It is described that stimulation by TNF-α results in incompletely matured DCs (semi-mature DCs) which induce peptide-specific IL-10–producing T cells in vivo and prevent EAE.
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Myeloid dendritic cell precursors generated from bone marrow suppress T cell responses via cell contact and nitric oxide production in vitro

TL;DR: The generation of MSC is described as myeloid DC precursors with potent suppressive activity on allogeneic and OVA‐specific CD4+ and CD8+ T cell responses in vitro preceding their development into immature DC.
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Dendritic Cells Matured With TNF can be Further Activated In Vitro and After Subcutaneous Injection In Vivo Which Converts Their Tolerogenicity Into Immunogenicity

TL;DR: It is shown that TNF/DC are not terminally differentiated but can still respond to the microbial stimulus lipopolysaccharide, which is important for selecting the appropriate injection route of human DC for tumor immunotherapy.
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Infliximab (Anti–Tumor Necrosis Factor α Antibody): A Novel, Highly Effective Treatment of Recalcitrant Subcorneal Pustular Dermatosis (Sneddon-Wilkinson Disease)

TL;DR: A 79-year old woman presented with a 7-year history of subcorneal pustular dermatosis (SPD), which was resistant to multiple therapeutic trials including colchicine, retinoids, systemic glucocorticosteroids, UV phototherapy, azathioprine, and azulfidine.
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Cutting Edge: Resistance to Apoptosis and Continuous Proliferation of Dendritic Cells Deficient for TNF Receptor-1

TL;DR: Prolonged survival of TNFR1−/− DC appears to be independent from NF-κB and Bcl-2 pathways and is rather enabled by the down-regulation of CD95, resulting in the resistance to CD95 ligand-induced apoptosis.