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Balam, Saidou [Author]; Kesselring, Rebecca [Author]; Eggenhofer, Elke [Author]; Blaimer, Stephanie [Author]; Evert, Katja [Author]; Evert, Matthias [Author]; Schlitt, Hans Jürgen [Author]; Geissler, Edward K. [Author]; Blijswijk, Janneke [Author]; Lee, Sonia [Author]; Reis e Sousa, Caetano [Author]; Brunner, Stefan M. [Author]; Fichtner-Feigl, Stefan [Author]

Cross‐presentation of dead‐cell‐associated antigens by DNGR‐1+ dendritic cells contributes to chronic allograft rejection in mice

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  • Media type: E-Book; Special Print
  • Title: Cross‐presentation of dead‐cell‐associated antigens by DNGR‐1+ dendritic cells contributes to chronic allograft rejection in mice
  • Contributor: Balam, Saidou [VerfasserIn]; Kesselring, Rebecca [VerfasserIn]; Eggenhofer, Elke [VerfasserIn]; Blaimer, Stephanie [VerfasserIn]; Evert, Katja [VerfasserIn]; Evert, Matthias [VerfasserIn]; Schlitt, Hans Jürgen [VerfasserIn]; Geissler, Edward K. [VerfasserIn]; Blijswijk, Janneke [VerfasserIn]; Lee, Sonia [VerfasserIn]; Reis e Sousa, Caetano [VerfasserIn]; Brunner, Stefan M. [VerfasserIn]; Fichtner-Feigl, Stefan [VerfasserIn]
  • imprint: Weinheim: Wiley, 2020
  • Published in: European journal of immunology ; 50, 12 (2020), 2041-2054
  • Extent: 1 Online-Ressource (14 Seiten); Illustrationen, Diagramme; 1 Datei (Supporting information)
  • Language: English
  • DOI: 10.1002/eji.201948501
  • ISSN: 1521-4141
  • Identifier:
  • Origination:
  • Footnote: Enthält eine pdf-Datei und eine zip-Datei
  • Description: Abstract: The purpose of this study was to elucidate whether DC NK lectin group receptor‐1 (DNGR‐1)‐dependent cross‐presentation of dead‐cell‐associated antigens occurs after transplantation and contributes to CD8+ T cell responses, chronic allograft rejection (CAR), and fibrosis. BALB/c or C57BL/6 hearts were heterotopically transplanted into WT, Clec9a−/−, or Batf3−/− recipient C57BL/6 mice. Allografts were analyzed for cell infiltration, CD8+ T cell activation, fibrogenesis, and CAR using immunohistochemistry, Western blot, qRT2‐PCR, and flow cytometry. Allografts displayed infiltration by recipient DNGR‐1+ DCs, signs of CAR, and fibrosis. Allografts in Clec9a−/− recipients showed reduced CAR (p < 0.0001), fibrosis (P = 0.0137), CD8+ cell infiltration (P < 0.0001), and effector cytokine levels compared to WT recipients. Batf3‐deficiency greatly reduced DNGR‐1+ DC‐infiltration, CAR (P < 0.0001), and fibrosis (P = 0.0382). CD8 cells infiltrating allografts of cytochrome C treated recipients, showed reduced production of CD8 effector cytokines (P < 0.05). Further, alloreactive CD8+ T cell response in indirect pathway IFN‐γ ELISPOT was reduced in Clec9a−/− recipient mice (P = 0.0283). Blockade of DNGR‐1 by antibody, similar to genetic elimination of the receptor, reduced CAR (P = 0.0003), fibrosis (P = 0.0273), infiltration of CD8+ cells (p = 0.0006), and effector cytokine levels. DNGR‐1‐dependent alloantigen cross‐presentation by DNGR‐1+ DCs induces alloreactive CD8+ cells that induce CAR and fibrosis. Antibody against DNGR‐1 can block this process and prevent CAR and fibrosis
  • Access State: Open Access