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@ARTICLE{Sicklinger:169666,
      author       = {F. Sicklinger and I. S. Meyer and X. Li and D. Radtke and
                      S. Dicks and M. P. Kornadt and C. Mertens and J. K. Meier
                      and K. J. Lavine and Y. Zhang and T. C. Kuhn and T.
                      Terzer$^*$ and J. Patel and M. Börries$^*$ and G. Schramm
                      and N. Frey and H. A. Katus and D. Voehringer and F.
                      Leuschner},
      title        = {{B}asophils balance healing after myocardial infarction via
                      {IL}-4/{IL}-13.},
      journal      = {The journal of clinical investigation},
      volume       = {131},
      number       = {13},
      issn         = {1558-8238},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2021-01488},
      pages        = {e136778},
      year         = {2021},
      abstract     = {The inflammatory response after myocardial infarction (MI)
                      is a precisely regulated process that greatly affects
                      subsequent remodeling. Here, we show that basophil
                      granulocytes infiltrated infarcted murine hearts, with a
                      peak occurring between days 3 and 7. Antibody-mediated and
                      genetic depletion of basophils deteriorated cardiac function
                      and resulted in enhanced scar thinning after MI.
                      Mechanistically, we found that basophil depletion was
                      associated with a shift from reparative Ly6Clo macrophages
                      toward increased numbers of inflammatory Ly6Chi monocytes in
                      the infarcted myocardium. Restoration of basophils in
                      basophil-deficient mice by adoptive transfer reversed this
                      proinflammatory phenotype. Cellular alterations in the
                      absence of basophils were accompanied by lower cardiac
                      levels of IL-4 and IL-13, two major cytokines secreted by
                      basophils. Mice with basophil-specific IL-4/IL-13 deficiency
                      exhibited a similarly altered myeloid response with an
                      increased fraction of Ly6Chi monocytes and aggravated
                      cardiac function after MI. In contrast, IL-4 induction in
                      basophils via administration of the glycoprotein IPSE/α-1
                      led to improved post-MI healing. These results in mice were
                      corroborated by the finding that initially low counts of
                      blood basophils in patients with acute MI were associated
                      with a worse cardiac outcome after 1 year, characterized by
                      a larger scar size. In conclusion, we show that basophils
                      promoted tissue repair after MI by increasing cardiac IL-4
                      and IL-13 levels.},
      keywords     = {Cardiology (Other) / Cardiovascular disease (Other) / Heart
                      failure (Other) / Innate immunity (Other)},
      cin          = {C060 / FR01},
      ddc          = {610},
      cid          = {I:(DE-He78)C060-20160331 / I:(DE-He78)FR01-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34196299},
      doi          = {10.1172/JCI136778},
      url          = {https://inrepo02.dkfz.de/record/169666},
}