@phdthesis{Heinrichs2018,
  author    = {Heinrichs, Susanne Margarete},
  title     = {Myocardial B-cell infiltration following occlusion of the left anterior descending artery in mice is driven by CXCL13},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-168554},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2018},
  abstract  = {Myocardial B-cell infiltration after LAD occlusion in mice is driven by CXCL13 After myocardial infarction, the immune system is activated and regulates wound healing and remodeling processes in the heart. While the role of T cells has been elucidated already, the function of B cells in myocardial infarction remained relatively unclear until now. It is, however, already known that B cells are of importance in healing processes in other tissues, for example in the skin. Our studies therefore addressed the role and function of B cells in healing and early remodeling processes in the myocardium after infarction. Under physiological conditions, only few B cells can be found in the heart. After myocardial infarction, however, which we modelled with a permanent ligation of the left anterior descending artery (LAD) in C57BL/6J mice, we could demonstrate that B lymphocytes accumulate in the early phase after tissue injury (days one to seven) in the myocardium. To detect B cells, we performed immunofluorescence stainings on cryosections of infarcted hearts using an anti-B220 antibody. Quantitative analysis of tissue infiltration revealed that B cells peaked at day seven. In flow cytometry, we further characterized the B cells infiltrating infarcted tissue. We found that most of them were mature B cells (IgM+, IgD+). Next, we wanted to outline a potential mechanism responsible for B-cell infiltration to the site of tissue injury. We therefore performed ELISA experiments revealing that CXCL13 was upregulated in scar tissue. Antibody-mediated neutralization of CXCL13 verifiably attenuated B-cell infiltration. Treated mice also showed - in the tendency - smaller infarct sizes and an improved survival. In conclusion, we could show that B lymphocytes infiltrate the myocardium after MI in mice following a local CXCL13 gradient and that it is, most likely, beneficial to inhibit this process.},
  subject      = {Maus},
  language  = {en}
}
@phdthesis{Herzele2001,
  author    = {Herzele, Karin},
  title     = {Untersuchung zur Spezifit{\"a}t von Autoantik{\"o}rpern bei Patienten mit linearer IgA Dermatose},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-1182267},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2001},
  abstract  = {Die lineare IgA Dermatose (LAD) ist eine subepidermal blasenbildende Erkrankung, die durch IgA-Ablagerungen an der kutanen Basalmembran charakterisiert ist. Die IgA-Antik{\"o}rper von LAD-Seren reagieren mit einem 97 kDa Protein, das aus der Epidermis extrahiert werden kann, und einem 120 kDa Protein, das von kultivierten Keratinozyten in das Kulturmedium sezerniert wird. Beide Antigene stellen Fragmente der extrazellul{\"a}ren Dom{\"a}ne des 180 kDa bull{\"o}sen Pemphigoid-Autoantigens (BP180, Typ XVII Kollagen) dar. Die vorliegende Studie ging der Frage nach, ob LAD-Seren mit der immunodominanten Region von BP180 (NC16A Region) unmittelbar an der Zellmemran der basalen Keratinozyten reagieren. Diese Region ist das Ziel der IgG-Antik{\"o}rper im Serum der meisten Patienten mit bull{\"o}sem Pemphigoid und Pemphigoid gestationis. Tats{\"a}chlich zeigte sich im Immunoblot bei 11 von 50 LAD-Patienten eine Reaktivit{\"a}t von IgA-Antik{\"o}rpern mit einer rekombinanten Form von BP180 NC16A. Wir fanden bez{\"u}glich Alter, Geschlecht und immunfluoreszenzoptischer Befunde keine signifikanten Unterschiede zwischen der BP180 NC16A-positiven Gruppe verglichen mit der Gruppe er LAD-Patienten, die keine Reaktivit{\"a}t mit NC16A aufwiesen. Weitere studien sollten die pathogenetische Relevanz der gegen BP180 NC16A gerichteten IgA-Autoantik{\"o}rper im Serum von LAD-Patienten untersuchen.},
  language  = {de}
}