% 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{Heindl:157717,
      author       = {Heindl, Steffanie and Ricci, Alessio and Carofiglio, Olga
                      and Zhou, Qihui and Arzberger, Thomas and Lenart, Nikolett
                      and Franzmeier, Nicolai and Hortobagyi, Tibor and Nelson,
                      Peter T and Stowe, Ann M and Denes, Adam and Edbauer, Dieter
                      and Liesz, Arthur},
      title        = {{C}hronic {T} cell proliferation in brains after stroke
                      could interfere with the efficacy of immunotherapies.},
      journal      = {Journal of experimental medicine},
      volume       = {218},
      number       = {8},
      issn         = {1540-9538},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DZNE-2021-01174},
      pages        = {e20202411},
      year         = {2021},
      abstract     = {Neuroinflammation is an emerging focus of translational
                      stroke research. Preclinical studies have demonstrated a
                      critical role for brain-invading lymphocytes in post-stroke
                      pathophysiology. Reducing cerebral lymphocyte invasion by
                      anti-CD49d antibodies consistently improves outcome in the
                      acute phase after experimental stroke models. However,
                      clinical trials testing this approach failed to show
                      efficacy in stroke patients for the chronic outcome 3 mo
                      after stroke. Here, we identify a potential mechanistic
                      reason for this phenomenon by detecting chronic T cell
                      accumulation-evading the systemic therapy-in the
                      post-ischemic brain. We observed a persistent accumulation
                      of T cells in mice and human autopsy samples for more than 1
                      mo after stroke. Cerebral T cell accumulation in the
                      post-ischemic brain was driven by increased local T cell
                      proliferation rather than by T cell invasion. This
                      observation urges re-evaluation of current immunotherapeutic
                      approaches, which target circulating lymphocytes for
                      promoting recovery after stroke.},
      keywords     = {Animals / Autopsy / Brain: immunology / Brain: pathology /
                      Brain Ischemia: drug therapy / Brain Ischemia: immunology /
                      Brain Ischemia: pathology / Cell Proliferation / Female /
                      Humans / Immunotherapy / Integrin alpha4: immunology /
                      Lymphocyte Count / Male / Mice, Inbred C57BL / Natalizumab:
                      pharmacology / Natalizumab: therapeutic use / Neuronal
                      Plasticity: drug effects / Recovery of Function: drug
                      effects / Stroke: immunology / Stroke: physiopathology /
                      Stroke: therapy / T-Lymphocytes: immunology},
      cin          = {AG Edbauer / AG Zhou},
      ddc          = {610},
      cid          = {I:(DE-2719)1110004 / I:(DE-2719)5000080},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34037669},
      pmc          = {pmc:PMC8160576},
      doi          = {10.1084/jem.20202411},
      url          = {https://pub.dzne.de/record/157717},
}