In JoVE (1)

Other Publications (4)

Articles by Volker Böhnert in JoVE

 JoVE Medicine

A Model to Simulate Clinically Relevant Hypoxia in Humans

1Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Bonn, 2Institute of Clinical Chemistry and Clinical Pharmacology, University of Bonn, 3Institute for Terrestrial and Aquatic Wildlife Research, University of Veterinary Medicine Hannover, 4Institute of Physiology 2, University of Bonn


JoVE 54933

Other articles by Volker Böhnert on PubMed

Morphologic and Molecular Characterization of Two Novel Krt71 (Krt2-6g) Mutations: Krt71rco12 and Krt71rco13

Mammalian Genome : Official Journal of the International Mammalian Genome Society. Dec, 2006  |  Pubmed ID: 17143583

We have analyzed two novel mouse mutant strains, Rco12 and Rco13, displaying a wavy pelage and curly vibrissae that have been identified in an ENU screen for dominant mutations affecting the pelage. The mutations were mapped to mouse Chromosome 15 and identified as missense point mutations in the first exon of the Krt71 (formerly called Krt2-6g) gene causing alterations of amino acid residue 143 from alanine to glycine (Rco12) and residue 146 from isoleucine to phenylalanine. The morphologic analyses demonstrated that both mutations cause identical phenotypes leading to the formation of filamentous aggregates in Henle's and Huxley's layers of the inner root sheath (IRS) of the hair follicle that leads to the bending of the hair shaft. Both novel mutations are located in the immediate vicinity of previously identified mutations in murine Krt71 that cause similar phenotypes and alter the helix initiation motif of the keratin. The characterization of these mutants demonstrates the importance of this Krt71 domain for the formation of linear IRS intermediate filaments.

Distinct Pathways of Antigen Uptake and Intracellular Routing in CD4 and CD8 T Cell Activation

Science (New York, N.Y.). Apr, 2007  |  Pubmed ID: 17463291

The mechanisms that allow antigen-presenting cells (APCs) to selectively present extracellular antigen to CD8+ effector T cells (cross-presentation) or to CD4+ T helper cells are not fully resolved. We demonstrated that APCs use distinct endocytosis mechanisms to simultaneously introduce soluble antigen into separate intracellular compartments, which were dedicated to presentation to CD8+ or CD4+ T cells. Specifically, the mannose receptor supplied an early endosomal compartment distinct from lysosomes, which was committed to cross-presentation. These findings imply that antigen does not require intracellular diversion to access the cross-presentation pathway, because it can enter the pathway already during endocytosis.

Improved Transplantation Outcome by Epigenetic Changes

Transplant Immunology. Jul, 2010  |  Pubmed ID: 20471480

Epigenetics and transplantation seem an odd couple. The influence of epigenetic changes on the immune response of the host following an organ graft is not one of the more obvious connections. However, modifying host immunity to a graft via epigenetic changes of immune related genes could have unexpected ramifications for therapy post transplantation. This review discusses various studies concerning the effects of epigenetic alterations on transplantation-associated pathologies. We present tools for improving transplantation outcome, such as histone deacetylase inhibition, DNA methyltransferase inhibition or venous systemic oxygen persufflation. This will allow a reduction of immunosuppressive medication, leading to fewer side effects. We also show, however, that much effort needs to be put into the elucidation of the molecular mechanisms underlying these advantageous effects. Taken together, altering epigenetics in transplanted organs will ultimately lead to a higher quality of life for transplant patients.

Targeted Activation of RNA Helicase Retinoic Acid-inducible Gene-I Induces Proimmunogenic Apoptosis of Human Ovarian Cancer Cells

Cancer Research. Jul, 2010  |  Pubmed ID: 20551064

Most malignant cells are poorly immunogenic and fail to elicit an effective antitumor immune response. In contrast, viral infections of cells are promptly detected and eliminated by the immune system. Viral recognition critically hinges on cytosolic nucleic acid receptors that include the proinflammatory RNA helicase retinoic acid-inducible gene-I (RIG-I). Here, we show that targeted delivery of RIG-I agonists induced ovarian cancer cells to upregulate HLA class I and to secrete the proinflammatory cytokines CXCL10, CCL5, interleukin-6, tumor necrosis factor-alpha, and IFN-beta. Ovarian cancer cells stimulated via RIG-I became apoptotic and were readily phagocytosed by monocytes and monocyte-derived dendritic cells, which in turn upregulated HLA class I/II and costimulatory molecules and released CXCL10 and IFN-alpha. Our findings offer proof of principle that mimicking viral infection in ovarian cancer cells triggers an immunogenic form of tumor cell apoptosis that may enhance immunotherapy of ovarian cancer.

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