@article{BogdanMollSolbachetal.1990,
  author    = {Bogdan, Christian and Moll, Heidrun and Solbach, Werner and R{\"o}llinghoff, Martin},
  title     = {Tumor necrosis factor-\(\alpha\) in combination with interferon-\(\gamma\), but not with interleukin 4 activates murine macrophages for elimination of Leishmania major amastigotes},
  volume    = {20},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31614},
  pages     = {1131 -- 1135},
  year      = {1990},
  abstract  = {We have previously shown that during an infection with Leishmania major, susceptible BALB/c mice, as opposed to mice of a resistant strain (C57BLl6), are primed by lipopolysaccharide for the production of high levels of tumor necrosis factor-\(\alpha\) (TNF-\(\alpha\)) which is known to be a potent maerophage M\(\Phi\) stimulator in other parasitic diseases. In the present study we investigated whether TNF-\(\alpha\) activates M\(\Phi\) for killing of L. major parasites. In the absence of interferon-y (IFN-\(\gamma\)) or lipopolysaccharide, TNF-\(\alpha\) (0.025-25000 U/ml) failed to activate peritoneal exudate M\(\Phi\) from BALB/c mice for killling of L. major amastigotes. In the presence of suboptimal doses of IFN-\(\gamma\) (5 or 10 Vlml), however, TNF-\(\alpha\) mediated a rapid elimination of intracellular parasites, which was highly significant compared to IFN-\(\gamma\) alone. Tbe combination of TNF with interleukin 4, in contrast, was inactive in this respect and allowed survival of intracellular parasites. From these data we conelude that the presence of IFN-\(\gamma\) is crucial for TNF-\(\alpha\)-mediated killing of L. major parasites by M\(\Phi\). Disease progression in susceptible mice therefore seems to be a consequence of a deficiency of IFN-\(\gamma\) and a predominance of interleukin 4 rather than the result of an excess amount of TNF-\(\alpha\).},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{MollBinoederBogdanetal.1990,
  author    = {Moll, Heidrun and Bin{\"o}der, Kerstin and Bogdan, Christian and Solbach, Werner and R{\"o}llinghoff, Martin},
  title     = {Production of tumour necrosis factor during murine cutaneous leishmaniasis},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61291},
  year      = {1990},
  abstract  = {We have assessed the role of tumour necrosis factor-a (TNF) during cutaneous leishmaniasis and demonstrated that significant levels of TNF were released by spleen cells from infected mice after in cirro restimulation with Leishmania major promastigotes. Spleen cells from both genetically resistant and genetically susceptible mice were equally capable of producing TNF. After challenge with bacterial endotoxin, TNF activity could also be demonstrated in the serum of L. mujor-infected mice and the titres correlated with the course of cutaneous disease in susceptible and resistant mice. TNF did not exert a direct leishmanicidal effect in uitro. Furthermore, our study indicated that macrophages are the source of L. major-induced TNF activity and that its elicitation is dependent on the presence of T cells. These findings suggest that TNF acts in concert with other cytokines produced during L. major infection and that its role depends on the composition of T cell subsets and cytokines present.},
  subject      = {Immunologie},
  language  = {en}
}
@article{SchleicherPaduchDebusetal.2016,
  author    = {Schleicher, Ulrike and Paduch, Katrin and Debus, Andrea and Obermeyer, Stephanie and K{\"o}nig, Till and Kling, Jessica C. and Ribechini, Eliana and Dudziak, Diana and Mougiakakos, Dimitrios and Murray, Peter J. and Ostuni, Renato and K{\"o}rner, Heinrich and Bogdan, Christian},
  title     = {TNF-Mediated Restriction of Arginase 1 Expression in Myeloid Cells Triggers Type 2 NO Synthase Activity at the Site of Infection},
  series = {Cell Reports},
  volume    = {15},
  journal   = {Cell Reports},
  number    = {5},
  doi       = {10.1016/j.celrep.2016.04.001},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164897},
  pages     = {1062-1075},
  year      = {2016},
  abstract  = {Neutralization or deletion of tumor necrosis factor (TNF) causes loss of control of intracellular pathogens in mice and humans, but the underlying mechanisms are incompletely understood. Here, we found that TNF antagonized alternative activation of macrophages and dendritic cells by IL-4. TNF inhibited IL-4-induced arginase 1 (Arg1) expression by decreasing histone acetylation, without affecting STAT6 phosphorylation and nuclear translocation. In Leishmania major-infected C57BL/6 wild-type mice, type 2 nitric oxide (NO) synthase (NOS2) was detected in inflammatory dendritic cells or macrophages, some of which co-expressed Arg1. In TNF-deficient mice, Arg1 was hyperexpressed, causing an impaired production of NO in situ. A similar phenotype was seen in L. major-infected BALB/c mice. Arg1 deletion in hematopoietic cells protected these mice from an otherwise lethal disease, although their disease-mediating T cell response (Th2, Treg) was maintained. Thus, deletion or TNF-mediated restriction of Arg1 unleashes the production of NO by NOS2, which is critical for pathogen control.},
  language  = {en}
}