Efficient B cell depletion via diphtheria toxin in CD19-Cre/iDTR mice

PLoS One. 2013;8(3):e60643. doi: 10.1371/journal.pone.0060643. Epub 2013 Mar 27.

Abstract

B cells were first discovered as antibody producing cells, as B-1 B cells and finally as effector cells. In recent years their capacity to serve as antigen presenting cells is increasingly appreciated, and better tools are needed to study their function. We have previously described a new mouse model, the iDTR mice, that allow for the Cre-mediated expression of the diphtheria toxin receptor, thus rendering cells that express the Cre-recombinase sensitivity to diphtheria toxin. Herein we describe a new mouse line, the B-DTR mice, where the CD19-Cre was crossed to the iDTR mice. B-DTR allows for the efficient and cost-effective depletion of different B cell subpopulations, but only partially plasma cells. These mice can therefore be used to study the importance of B cells versus plasma cells in different immune responses and autoimmune diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD19 / metabolism*
  • B-Lymphocytes / cytology
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / metabolism*
  • Bacterial Proteins / metabolism
  • Diphtheria Toxin / pharmacology*
  • Heparin-binding EGF-like Growth Factor
  • Immunoglobulins / blood
  • Integrases / metabolism*
  • Intercellular Signaling Peptides and Proteins / metabolism*
  • Luminescent Proteins / metabolism
  • Lymphocyte Count
  • Lymphocyte Depletion*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Plasma Cells / drug effects
  • Plasma Cells / metabolism
  • Syndecan-1 / metabolism

Substances

  • Antigens, CD19
  • Bacterial Proteins
  • Diphtheria Toxin
  • Hbegf protein, mouse
  • Heparin-binding EGF-like Growth Factor
  • Immunoglobulins
  • Intercellular Signaling Peptides and Proteins
  • Luminescent Proteins
  • Syndecan-1
  • yellow fluorescent protein, Bacteria
  • Cre recombinase
  • Integrases

Grants and funding

This study was supported by funds via the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG) graduate school GRK 1043 to AW and by the DFG grants WA 1600/3-1, SFB/TR 52 and the DFG research group FOR1336 to AW. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.