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@ARTICLE{Cheng:125631,
      author       = {F. Cheng and L. Twardowski and K. Reifenberg$^*$ and K.
                      Winter and A. Canisius and E. Pross and J. Fan and E.
                      Schmitt and L. D. Shultz and K. J. Lackner and M. Torzewski},
      title        = {{C}ombined {B}, {T} and {NK} {C}ell {D}eficiency
                      {A}ccelerates {A}therosclerosis in {BALB}/c {M}ice.},
      journal      = {PLoS one},
      volume       = {11},
      number       = {8},
      issn         = {1932-6203},
      address      = {Lawrence, Kan.},
      publisher    = {PLoS},
      reportid     = {DKFZ-2017-01757},
      pages        = {e0157311 -},
      year         = {2016},
      abstract     = {This study focused on the unique properties of both the
                      Ldlr knockout defect (closely mimicking the human situation)
                      and the BALB/c (C) inbred mouse strain (Th-2 slanted immune
                      response). We generated two immunodeficient strains with
                      severe combined B- and T-cell immunodeficiency with or
                      without a complete lack of natural killer cells to revisit
                      the role of adaptive immune responses on atherogenesis.
                      C-Ldlr-/- Rag1-/- mice, which show severe combined B- and
                      T-cell immunodeficiency and C-Ldlr-/- Rag1-/- Il2rg-/- mice,
                      which combine the T- and B-cell defect with a complete lack
                      of natural killer cells and inactivation of multiple
                      cytokine signalling pathways were fed an atherogenic Western
                      type diet (WTD). Both B6-Ldlr-/- and C-Ldlr-/-
                      immunocompetent mice were used as controls. Body weights and
                      serum cholesterol levels of both immunodeficient strains
                      were significantly increased compared to C-Ldlr-/- controls,
                      except for cholesterol levels of C-Ldlr-/- Rag1-/- double
                      mutants after 12 weeks on the WTD. Quantification of the
                      aortic sinus plaque area revealed that both strains of
                      immunodeficient mice developed significantly more
                      atherosclerosis compared to C-Ldlr-/- controls after 24
                      weeks on the WTD. Increased atherosclerotic lesion
                      development in C-Ldlr-/- Rag1-/- Il2rg-/- triple mutants was
                      associated with significantly increased numbers of
                      macrophages and significantly decreased numbers of smooth
                      muscle cells compared to both C-Ldlr-/- wild type and
                      C-Ldlr-/- Rag1-/- double mutants pointing to a plaque
                      destabilizing effect of NK cell loss. Collectively, the
                      present study reveals a previously unappreciated complexity
                      with regard to the impact of lymphocytes on lipoprotein
                      metabolism and the role of lymphocyte subsets in plaque
                      composition.},
      keywords     = {Lipoproteins (NLM Chemicals) / Receptors, LDL (NLM
                      Chemicals) / Triglycerides (NLM Chemicals) / Cholesterol
                      (NLM Chemicals)},
      cin          = {W410},
      ddc          = {500},
      cid          = {I:(DE-He78)W410-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27564380},
      pmc          = {pmc:PMC5001715},
      doi          = {10.1371/journal.pone.0157311},
      url          = {https://inrepo02.dkfz.de/record/125631},
}