% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Haupeltshofer:872748,
      author       = {Haupeltshofer, Steffen and Leichsenring, Teresa and Berg,
                      Sarah and Pedreiturria, Xiomara and Joachim, Stephanie C.
                      and Tischoff, Iris and Otte, Jan-Michel and Bopp, Tobias and
                      Fantini, Massimo C. and Esser, Charlotte and Willbold,
                      Dieter and Gold, Ralf and Faissner, Simon and Kleiter, Ingo},
      title        = {{S}mad7 in intestinal {CD}4 + {T} cells determines
                      autoimmunity in a spontaneous model of multiple sclerosis},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {116},
      number       = {51},
      issn         = {1091-6490},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {FZJ-2020-00226},
      pages        = {25860 - 25869},
      year         = {2019},
      abstract     = {Environmental triggers acting at the intestinal barrier are
                      thought to contribute to the initiation of autoimmune
                      disorders. The transforming growth factor beta inhibitor
                      Smad7 determines the phenotype of CD4+ T cells. We
                      hypothesized that Smad7 in intestinal CD4+ T cells controls
                      initiation of opticospinal encephalomyelitis (OSE), a murine
                      model of multiple sclerosis (MS), depending on the presence
                      of gut microbiota. Smad7 was overexpressed or deleted in OSE
                      CD4+ T cells to determine the effect on clinical
                      progression, T cell differentiation, and T cell migration
                      from the intestine to the central nervous system (CNS).
                      Smad7 overexpression worsened the clinical course of OSE and
                      increased CNS inflammation and demyelination. It favored
                      expansion of intestinal CD4+ T cells toward an inflammatory
                      phenotype and migration of intestinal CD4+ T cells to the
                      CNS. Intestinal biopsies from MS patients revealed decreased
                      transforming growth factor beta signaling with a shift
                      toward inflammatory T cell subtypes. Smad7 in intestinal T
                      cells might represent a valuable therapeutic target for MS
                      to achieve immunologic tolerance in the intestine and
                      suppress CNS inflammation.},
      cin          = {ICS-6},
      ddc          = {500},
      cid          = {I:(DE-Juel1)ICS-6-20110106},
      pnm          = {553 - Physical Basis of Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31796589},
      UT           = {WOS:000503281500070},
      doi          = {10.1073/pnas.1905955116},
      url          = {https://juser.fz-juelich.de/record/872748},
}