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@ARTICLE{Huard:274560,
      author       = {A. Huard and C. Wilmes and A. Kiprina and C. Netzer and G.
                      Palmer and B. Brüne$^*$ and A. Weigert$^*$},
      title        = {{C}ell {I}ntrinsic {IL}-38 {A}ffects {B} {C}ell
                      {D}ifferentiation and {A}ntibody {P}roduction.},
      journal      = {International journal of molecular sciences},
      volume       = {24},
      number       = {6},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2023-00637},
      pages        = {5676},
      year         = {2023},
      abstract     = {IL-38 is an IL-1 family receptor antagonist with an
                      emerging role in chronic inflammatory diseases. IL-38
                      expression has been mainly observed not only in epithelia,
                      but also in cells of the immune system, including
                      macrophages and B cells. Given the association of both IL-38
                      and B cells with chronic inflammation, we explored if IL-38
                      affects B cell biology. IL-38-deficient mice showed higher
                      amounts of plasma cells (PC) in lymphoid organs but,
                      conversely, lower levels of plasmatic antibody titers.
                      Exploring underlying mechanisms in human B cells revealed
                      that exogenously added IL-38 did not significantly affect
                      early B cell activation or differentiation into plasma
                      cells, even though IL-38 suppressed upregulation of CD38.
                      Instead, IL-38 mRNA expression was transiently upregulated
                      during the differentiation of human B cells to plasma cells
                      in vitro, and knocking down IL-38 during early B cell
                      differentiation increased plasma cell generation, while
                      reducing antibody production, thus reproducing the murine
                      phenotype. Although this endogenous role of IL-38 in B cell
                      differentiation and antibody production did not align with
                      an immunosuppressive function, autoantibody production
                      induced in mice by repeated IL-18 injections was enhanced in
                      an IL-38-deficient background. Taken together, our data
                      suggest that cell-intrinsic IL-38 promotes antibody
                      production at baseline but suppresses the production of
                      autoantibodies in an inflammatory context, which may
                      partially explain its protective role during chronic
                      inflammation.},
      keywords     = {B cell differentiation (Other) / IL-1 family (Other) /
                      IL-38 (Other) / antibodies (Other) / autoimmunity (Other)},
      cin          = {FM01},
      ddc          = {540},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36982750},
      doi          = {10.3390/ijms24065676},
      url          = {https://inrepo02.dkfz.de/record/274560},
}