@article{RiquelmeHaarerKammleretal.2018,
  author    = {Riquelme, Paloma and Haarer, Jan and Kammler, Anja and Walter, Lisa and Tomiuk, Stefan and Ahrens, Norbert and Wege, Anja K. and Goecze, Ivan and Zecher, Daniel and Banas, Bernhard and Spang, Rainer and F{\"a}ndrich, Fred and Lutz, Manfred B. and Sawitzki, Birgit and Schlitt, Hans J. and Ochando, Jordi and Geissler, Edward K. and Hutchinson, James A.},
  title     = {TIGIT\(^+\) iTregs elicited by human regulatory macrophages control T cell immunity},
  series = {Nature Communications},
  volume    = {9},
  journal   = {Nature Communications},
  number    = {9},
  doi       = {10.1038/s41467-018-05167-8},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-226321},
  pages     = {2858, 1-18},
  year      = {2018},
  abstract  = {Human regulatory macrophages (Mreg) have shown early clinical promise as a cell-based adjunct immunosuppressive therapy in solid organ transplantation. It is hypothesised that recipient CD4(+) T cell responses are actively regulated through direct allorecognition of donor-derived Mregs. Here we show that human Mregs convert allogeneic CD4(+) T cells to IL-10-producing, TIGIT(+) FoxP3(+)-induced regulatory T cells that non-specifically suppress bystander T cells and inhibit dendritic cell maturation. Differentiation of Mreg-induced Tregs relies on multiple non-redundant mechanisms that are not exclusive to interaction of Mregs and T cells, including signals mediated by indoleamine 2,3-dioxygenase, TGF-beta, retinoic acid, Notch and progestagen-associated endometrial protein. Preoperative administration of donor-derived Mregs to living-donor kidney transplant recipients results in an acute increase in circulating TIGIT(+) Tregs. These results suggest a feed-forward mechanism by which Mreg treatment promotes allograft acceptance through rapid induction of direct-pathway Tregs.},
  language  = {en}
}
@article{BalaRonchiPichletal.2014,
  author    = {Bala, Margarita and Ronchi, Cristina L. and Pichl, Josef and Wild, Vanessa and Kircher, Stefan and Allolio, Bruno and Hahner, Stefanie},
  title     = {Suspected metastatic adrenocortical carcinoma revealing as pulmonary Kaposi sarcoma in adrenal Cushing's syndrome},
  doi       = {10.1186/1472-6823-14-63},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-110553},
  year      = {2014},
  abstract  = {Background Kaposi sarcoma (KS) is a malignant disease most commonly diagnosed in the setting of a human immunodeficiency virus (HIV) infection and in patients receiving immunosuppressive treatment. Pulmonary KS has never been reported in association with endogenous Cushing's syndrome (CS). Case presentation A 60-year-old woman presented with symptoms and signs of CS. Adrenal CS was confirmed by standard biochemical evaluation. Imaging revealed a right adrenal lesion (diameter 3.5 cm) and multiple pulmonary nodules, suggesting a cortisol-secreting adrenal carcinoma with pulmonary metastases. The patient underwent right adrenalectomy with a pathohistological diagnosis of an adrenal adenoma. Subsequent thoracoscopic wedge resection of one lung lesion revealed pulmonary KS with positive immunostaining for human herpes virus 8 (HHV-8). HIV-serology was negative. Hydrocortisone replacement was initiated for secondary adrenal insufficiency after surgery. Post-operative follow up imaging showed complete remission of all KS-related pulmonary nodules solely after resolution of hypercortisolism. Conclusion KS may occur in the setting of endogenous CS and may go into remission after cure of hypercortisolism without further specific treatment.},
  language  = {en}
}