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@ARTICLE{Culina:136022,
      author       = {S. Culina and A. I. Lalanne and G. Afonso and K.
                      Cerosaletti and S. Pinto$^*$ and G. Sebastiani and K.
                      Kuranda and L. Nigi and A. Eugster and T. Østerbye and A.
                      Maugein and J. E. McLaren and K. Ladell and E. Larger and
                      J.-P. Beressi and A. Lissina and V. Appay and H. W. Davidson
                      and S. Buus and D. A. Price and M. Kuhn and E. Bonifacio and
                      M. Battaglia and S. Caillat-Zucman and F. Dotta and R.
                      Scharfmann and B. Kyewski$^*$ and R. Mallone and J.-C. Carel
                      and N. Tubiana-Rufi and L. Martinerie and A. Poidvin and E.
                      JacqzAigrain and L. Corvez and V. Berruer and J.-F. Gautier
                      and B. Baz and N. Haddadi and F. Andreelli and C. Amouyal
                      and S. Jaqueminet and O. Bourron and E. Dasque and A.
                      Hartemann and A. Lemoine-Yazigi and D. Dubois-Laforgue and
                      F. Travert and M. Feron and P. Rolland and V. Vignali and M.
                      Marre and P. Chanson and C. Briet and P.-J. Guillausseau and
                      L. Ait-Bachir and C. Collet and F. Beziaud and V.
                      Desforges-Bullet and G. Petit-Aubert and S. Christin-Maitre
                      and B. Fève and C. Vatier and N. Bourcigaux and C.
                      Lautridou and N. Lahlou and P. Bakouboula and C. Elie and H.
                      Morel and J.-M. Treluyer and M.-C. Gagnerault and C.
                      Maillard and A. Jones},
      collaboration = {I. S. Group},
      title        = {{I}slet-reactive {CD}8+ {T} cell frequencies in the
                      pancreas, but not in blood, distinguish type 1 diabetic
                      patients from healthy donors.},
      journal      = {Science immunology},
      volume       = {3},
      number       = {20},
      issn         = {2470-9468},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DKFZ-2018-00722},
      pages        = {eaao4013 -},
      year         = {2018},
      abstract     = {The human leukocyte antigen-A2 (HLA-A2)-restricted zinc
                      transporter 8186-194 (ZnT8186-194) and other islet epitopes
                      elicit interferon-γ secretion by CD8+ T cells
                      preferentially in type 1 diabetes (T1D) patients compared
                      with controls. We show that clonal ZnT8186-194-reactive CD8+
                      T cells express private T cell receptors and display
                      equivalent functional properties in T1D and healthy
                      individuals. Ex vivo analyses further revealed that CD8+ T
                      cells reactive to ZnT8186-194 and other islet epitopes
                      circulate at similar frequencies and exhibit a predominantly
                      naïve phenotype in age-matched T1D and healthy donors.
                      Higher frequencies of ZnT8186-194-reactive CD8+ T cells with
                      a more antigen-experienced phenotype were detected in
                      children versus adults, irrespective of disease status.
                      Moreover, some ZnT8186-194-reactive CD8+ T cell clonotypes
                      were found to cross-recognize a Bacteroides stercoris
                      mimotope. Whereas ZnT8 was poorly expressed in thymic
                      medullary epithelial cells, variable thymic expression
                      levels of islet antigens did not modulate the peripheral
                      frequency of their cognate CD8+ T cells. In contrast,
                      ZnT8186-194-reactive cells were enriched in the pancreata of
                      T1D patients versus nondiabetic and type 2 diabetic
                      individuals. Thus, islet-reactive CD8+ T cells circulate in
                      most individuals but home to the pancreas preferentially in
                      T1D patients. We conclude that the activation of this common
                      islet-reactive T cell repertoire and progression to T1D
                      likely require defective peripheral immunoregulation and/or
                      a proinflammatory islet microenvironment.},
      cin          = {D090 ; D090},
      ddc          = {610},
      cid          = {I:(DE-He78)D090-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29429978},
      pmc          = {pmc:PMC5874133},
      doi          = {10.1126/sciimmunol.aao4013},
      url          = {https://inrepo02.dkfz.de/record/136022},
}