@article{ReckeKonitzerLemckeetal.2018,
  author    = {Recke, Andreas and Konitzer, Sarah and Lemcke, Susanne and Freitag, Miriam and Sommer, Nele Maxi and Abdelhady, Mohammad and Amoli, Mahsa M. and Benoit, Sandrine and El-Chennawy, Farha and Eldarouti, Mohammad and Eming, R{\"u}diger and Gl{\"a}ser, Regine and G{\"u}nther, Claudia and Hadaschik, Eva and Homey, Bernhard and Lieb, Wolfgang and Peitsch, Wiebke K. and Pf{\"o}hler, Claudia and Robati, Reza M. and Saeedi, Marjan and S{\´a}rdy, Mikl{\´o}s and Sticherling, Michael and Uzun, Soner and Worm, Margitta and Zillikens, Detlef and Ibrahim, Saleh and Vidarsson, Gestur and Schmidt, Enno},
  title     = {The p.Arg435His Variation of IgG3 With High Affinity to FcRn Is Associated With Susceptibility for Pemphigus Vulgaris-Analysis of Four Different Ethnic Cohorts},
  series = {frontiers in Immunology},
  volume    = {9},
  journal   = {frontiers in Immunology},
  doi       = {10.3389/fimmu.2018.01788},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-225073},
  pages     = {1788, 1-8},
  year      = {2018},
  abstract  = {IgG3 is the IgG subclass with the strongest effector functions among all four IgG subclasses and the highest degree of allelic variability among all constant immunoglobulin genes. Due to its genetic position, IgG3 is often the first isotype an antibody switches to before IgG1 or IgG4. Compared with the other IgG subclasses, it has a reduced half-life which is probably connected to a decreased affinity to the neonatal Fc receptor (FcRn). However, a few allelic variants harbor an amino acid replacement of His435 to Arg that reverts the half-life of the resulting IgG3 to the same level as the other IgG subclasses. Because of its functional impact, we hypothesized that the p.Arg435His variation could be associated with susceptibility to autoantibody-mediated diseases like pemphigus vulgaris (PV) and bullous pemphigoid (BP). Using a set of samples from German, Turkish, Egyptian, and Iranian patients and controls, we were able to demonstrate a genetic association of the p.Arg435His variation with PV risk, but not with BP risk. Our results suggest a hitherto unknown role for the function of IgG3 in the pathogenesis of PV.},
  subject      = {Diagnose},
  language  = {en}
}
@article{SchiererOstaleckiZinseretal.2018,
  author    = {Schierer, Stefan and Ostalecki, Christian and Zinser, Elisabeth and Lamprecht, Ricarda and Plosnita, Bianca and Stich, Lena and Doerrie, Jan and Lutz, Manfred B and Schuler, Gerold and Baur, Andreas S},
  title     = {Extracellular vesicles from mature dendritic cells (DC) differentiate monocytes into immature DC},
  series = {Life Science Alliance},
  volume    = {1},
  journal   = {Life Science Alliance},
  number    = {6},
  doi       = {10.26508/lsa.201800093},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-228587},
  pages     = {e201800093, 1-17},
  year      = {2018},
  abstract  = {During inflammation, murine and human monocytes can develop into dendritic cells (DC), but this process is not entirely understood. Here, we demonstrate that extracellular vesicles (EV) secreted by mature human DC (maDC) differentiate peripheral monocytes into immature DC, expressing a unique marker pattern, including 6-sulfo LacNAc (slan), Zbtb46, CD64, and CD14. While EV from both maDC and immature DC differentiated monocytes similar to GM-CSF/IL-4 stimulation, only maDC-EV produced precursors, which upon maturation stimulus developed into T-cell-activating and IL-12p70-secreting maDC. Mechanistically, maDC-EV induced cell signaling through GM-CSF, which was abundant in EV as were IL-4 and other cytokines and chemokines. When injected into the mouse skin, murine maDC-EV attracted immune cells including monocytes that developed activation markers typical for inflammatory cells. Skin-injected EV also reached lymph nodes, causing a similar immune cell infiltration. We conclude that DC-derived EV likely serve to perpetuate an immune reaction and may contribute to chronic inflammation.},
  language  = {en}
}