@article{NicolaiPoetschkeSchmoeckeletal.2020,
  author    = {Oliver Nicolai and Christian P{\"o}tschke and Katrin Schmoeckel and Murthy N. Darisipudi and Julia van der Linde and Dina Raafat and Barbara M. Br{\"o}ker},
  title     = {Antibody Production in Murine Polymicrobial Sepsis—Kinetics and Key Players},
  series   = {Frontiers in Immunology},
  volume    = {11},
  publisher = {Frontiers Media S.A.},
  issn      = {1664-3224},
  doi       = {10.3389/fimmu.2020.00828},
  url       = {https://nbn-resolving.org/urn:nbn:de:gbv:9-opus-36805},
  year      = {2020},
  abstract  = {Although antigen-specific priming of antibody responses is impaired during sepsis, there is nevertheless a strong increase in IgM and IgG serum concentrations. Using colon ascendens stent peritonitis (CASP), a mouse model of polymicrobial abdominal sepsis, we observed substantial increases in IgM as well as IgG of all subclasses, starting at day 3 and peaking 2 weeks after sepsis induction. The dominant source of antibody-secreting cells was by far the spleen, with a minor contribution of the mesenteric lymph nodes. Remarkably, sepsis induction in splenectomized mice did not change the dynamics of the serum IgM/IgG reaction, indicating that the marginal zone B cells, which almost exclusively reside in the spleen, are dispensable in such a setting. Hence, in systemic bacterial infection, the function of the spleen as dominant niche of antibody-producing cells can be compensated by extra-splenic B cell populations as well as other lymphoid organs. Depletion of CD4+ T cells did not affect the IgM response, while it impaired IgG generation of all subclasses with the exception of IgG3. Taken together, our data demonstrate that the robust class-switched antibody response in sepsis encompasses both T cell-dependent and -independent components.},
  language  = {en}
}