@article{MilanezAlmeidaUlasPasztoietal.2015,
  author    = {Milanez-Almeida, P. and Ulas, T. and Pasztoi, M. and Glage, S. and Schughart, K. and Lutz, M. B. and Schultze, J. L. and Huehn, J.},
  title     = {CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells with suppressive activity towards T cells accumulate in lungs of influenza A virus-infected mice},
  series = {European Journal of Microbiology and Immunology},
  volume    = {5},
  journal   = {European Journal of Microbiology and Immunology},
  number    = {4},
  doi       = {10.1556/1886.2015.00038},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-149583},
  pages     = {246-255},
  year      = {2015},
  abstract  = {Influenza A virus (IAV) infection causes an acute respiratory disease characterized by a strong inflammatory immune response and severe immunopathology. Proinflammatory mechanisms are well described in the murine IAV infection model, but less is known about the mechanisms leading to the resolution of inflammation. Here, we analyzed the contribution of CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells to this process. An accumulation of CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells within the lungs was observed during the course of IAV infection. Phenotypic characterization of these CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells by flow cytometry and RNA-Seq revealed an activated phenotype showing both pro- and anti-inflammatory features, including the expression of inducible nitric oxide synthase (iNOS) by a fraction of cells in an IFN-γ-dependent manner. Moreover, CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells isolated from lungs of IAV-infected animals displayed suppressive activity when tested in vitro, and iNOS inhibitors could abrogate this suppressive activity. Collectively, our data suggest that during IAV infection, CD11b\(^{+}\)Ly6C\(^{++}\)Ly6G\(^{-}\) cells acquire immunoregulatory function, which might contribute to the prevention of pathology during this life-threatening disease.},
  language  = {en}
}
@article{KoutsilieriLutzScheller2013,
  author    = {Koutsilieri, E. and Lutz, M. B. and Scheller, C.},
  title     = {Autoimmunity, dendritic cells and relevance for Parkinson's disease},
  series = {Journal of Neural Transmission},
  volume    = {120},
  journal   = {Journal of Neural Transmission},
  doi       = {10.1007/s00702-012-0842-7},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132308},
  pages     = {75-81},
  year      = {2013},
  abstract  = {Innate and adaptive immune responses in neurodegenerative diseases have become recently a focus of research and discussions. Parkinson's disease (PD) is a neurodegenerative disorder without known etiopathogenesis. The past decade has generated evidence for an involvement of the immune system in PD pathogenesis. Both inflammatory and autoimmune mechanisms have been recognized and studies have emphasized the role of activated microglia and T-cell infiltration. In this short review, we focus on dendritic cells, on their role in initiation of autoimmune responses, we discuss aspects of neuroinflammation and autoimmunity in PD, and we report new evidence for the involvement of neuromelanin in these processes.},
  language  = {en}
}