@article{MollFuchsBlanketal.1993,
  author    = {Moll, Heidrun and Fuchs, Harald and Blank, Christine and R{\"o}llinghoff, Martin},
  title     = {Langerhans cells transport Leishmania major from the infected skin to the draining lymph node for presentation to antigen-specific T cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-46023},
  year      = {1993},
  abstract  = {No abstract available},
  subject      = {Immunologie},
  language  = {en}
}
@article{BlankFuchsRappersbergeretal.1993,
  author    = {Blank, Christine and Fuchs, Harald and Rappersberger, Klemens and R{\"o}llinghoff, Martin and Moll, Heidrun},
  title     = {Parasitism of epidermal Langerhans cells in experimental cutaneous leishmaniasis with Leishmania major},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-45850},
  year      = {1993},
  abstract  = {Murine epidermal Langerhans cells (LC) have been demonstrated to stimulate a vigorous T cell response to Leishmania major, a cause of human cutaneous leishmaniasis. It was therefore of interest to analyze whether LC can take up viable parasites. Epidermal cells were obtained from mouse ear skin for incubation with L. major and subsequent detection of intracellular parasites by cytochemistry. Freshly isolated LC, but not cultured LC, phagocytosed L. major and the uptake was inhibited by antibodies to the complement receptor type 3. Electron microscopic studies revealed the presence of viable amastigotes within Le. Moreover, with double-Iabeling techniques, L. major-containing LC could also be detected in infected skin. The results demonstrate that LC can internalize L. major. Since the number of organisms per infected LC remained consistently low, the prime task of LC may not be the promotion of parasite spreading but the presentation of L. major antigen to T cells and, thus, the regulation of the cellular immunity during cutaneous leishmaniasis.},
  language  = {en}
}
@article{MollMuellerGillitzeretal.1991,
  author    = {Moll, Heidrun and M{\"u}ller, Christoph and Gillitzer, Reinhard and Fuchs, Harald and R{\"o}llinghoff, Martin and Simon, Markus M. and Kramer, Michael D.},
  title     = {Expression of T-cell-associated serine proteinase-1 during murine Leishmania major infection correlates with susceptibility to disease},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61311},
  year      = {1991},
  abstract  = {The expression of T-cell-associated serine proteinase 1 (MTSP-1) in vivo during Leishmania major infection was analyzed in genetically resistant C57BL/6 mice and in genetically susceptible BALB/c mice. Using a monoclonal antibody as well as an RNA probe specific for MTSP-1 to stain tissue sections, we found T cells expressing MTSP-1 in skin lesions and spleens of mice of both strains. In skin lesions, MTSP-1-positive T cells could be detected as early as 3 days after infection. Most importantly, the frequency of T cells expressing MTSP-1 was significantly higher in susceptible BALB/c mice than in resistant C57BL/6 mice. These findings suggest that MTSP-1 is associated with disease-promoting T cells and that it may be an effector molecule involved in the pathogenesis of cutaneous leishmaniasis.},
  subject      = {Biologie},
  language  = {en}
}
@article{KleinschnitzGrundWingleretal.2010,
  author    = {Kleinschnitz, Christoph and Grund, Henrike and Wingler, Kirstin and Armitage, Melanie E. and Jones, Emma and Mittal, Manish and Barit, David and Schwarz, Tobias and Geis, Christian and Kraft, Peter and Barthel, Konstanze and Schuhmann, Michael K. and Herrmann, Alexander M. and Meuth, Sven G. and Stoll, Guido and Meurer, Sabine and Schrewe, Anja and Becker, Lore and Gailus-Durner, Valerie and Fuchs, Helmut and Klopstock, Thomas and de Angelis, Martin Hrabe and Jandeleit-Dahm, Karin and Shah, Ajay M. and Weissmann, Norbert and Schmidt, Harald H. H. W.},
  title     = {Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-68416},
  year      = {2010},
  abstract  = {Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90\% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox42/2) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox42/2 mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy.},
  subject      = {Schlaganfall},
  language  = {en}
}