@article{ArdeltEbbingAdamsetal.2015,
  author    = {Ardelt, Peter U. and Ebbing, Jan and Adams, Fabian and Reiss, Cora and Arap, Wadih and Pasqualini, Renata and Bachmann, Alexander and Wetterauer, Ulrich and Riedmiller, Hubertus and Kneitz, Burkard},
  title     = {An anti-ubiquitin antibody response in transitional cell carcinoma of the urinary bladder},
  series = {PLoS ONE},
  volume    = {10},
  journal   = {PLoS ONE},
  number    = {3},
  doi       = {10.1371/journal.pone.0118646},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-143711},
  pages     = {e0118646},
  year      = {2015},
  abstract  = {Background To use combinatorial epitope mapping ("fingerprinting") of the antibody response to identify targets of the humoral immune response in patients with transitional cell carcinoma (TCC) of the bladder. Methods A combinatorial random peptide library was screened on the circulating pool of immunoglobulins purified from an index patient with a high risk TCC (pTa high grade plus carcinoma in situ) to identify corresponding target antigens. A patient cohort was investigated for antibody titers against ubiquitin. Results We selected, isolated, and validated an immunogenic peptide motif from ubiquitin as a dominant epitope of the humoral response. Patients with TCC had significantly higher antibody titers against ubiquitin than healthy donors (p<0.007), prostate cancer patients (p<0.0007), and all patients without TCC taken together (p<0.0001). Titers from superficial tumors were not significantly different from muscle invasive tumors (p = 0.0929). For antibody response against ubiquitin, sensitivity for detection of TCC was 0.44, specificity 0.96, positive predictive value 0.96 and negative predictive value 0.41. No significant titer changes were observed during the standard BCG induction immunotherapy. Conclusions This is the first report to demonstrate an anti-ubiquitin antibody response in patients with TCC. Although sensitivity of antibody production was low, a high specificity and positive predictive value make ubiquitin an interesting candidate for further diagnostic and possibly immune modulating studies.},
  language  = {en}
}
@article{AueEnglertHarreretal.2023,
  author    = {Aue, Annemarie and Englert, Nils and Harrer, Leon and Schwiering, Fabian and Gaab, Annika and K{\"o}nig, Peter and Adams, Ralf and Schmidtko, Achim and Friebe, Andreas and Groneberg, Dieter},
  title     = {NO-sensitive guanylyl cyclase discriminates pericyte-derived interstitial from intra-alveolar myofibroblasts in murine pulmonary fibrosis},
  series = {Respiratory Research},
  volume    = {24},
  journal   = {Respiratory Research},
  doi       = {10.1186/s12931-023-02479-2},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-357805},
  year      = {2023},
  abstract  = {Background The origin of αSMA-positive myofibroblasts, key players within organ fibrosis, is still not fully elucidated. Pericytes have been discussed as myofibroblast progenitors in several organs including the lung. Methods Using tamoxifen-inducible PDGFRβ-tdTomato mice (PDGFRβ-CreERT2; R26tdTomato) lineage of lung pericytes was traced. To induce lung fibrosis, a single orotracheal dose of bleomycin was given. Lung tissue was investigated by immunofluorescence analyses, hydroxyproline collagen assay and RT-qPCR. Results Lineage tracing combined with immunofluorescence for nitric oxide-sensitive guanylyl cyclase (NO-GC) as marker for PDGFRβ-positive pericytes allows differentiating two types of αSMA-expressing myofibroblasts in murine pulmonary fibrosis: (1) interstitial myofibroblasts that localize in the alveolar wall, derive from PDGFRβ+ pericytes, express NO-GC and produce collagen 1. (2) intra-alveolar myofibroblasts which do not derive from pericytes (but express PDGFRβ de novo after injury), are negative for NO-GC, have a large multipolar shape and appear to spread over several alveoli within the injured areas. Moreover, NO-GC expression is reduced during fibrosis, i.e., after pericyte-to-myofibroblast transition. Conclusion In summary, αSMA/PDGFRβ-positive myofibroblasts should not be addressed as a homogeneous target cell type within pulmonary fibrosis.},
  language  = {en}
}