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Dendritic-Like Cells from relB Mutant Mice

  • Lisa Dimolfetto
  • Christina Reilly
  • Qun Wei
  • David Lo
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 417)

Abstract

Mice deficient in the NF-κB transcription factor relB appear to have defects in the production of mature dendritic cells, as secondary lymphoid tissues are absent, and spleen cells show a significant loss of antigen presenting function. Moreover, the thymus appears to be impaired in negative selection, and immune responses in vivo are poor. Since dendritic cell precursors such as skin Langerhans cells appear to be normal, we sought information on the nature of the dendritic cell defect in these mice. Cultures of mutant bone marrow in the presence of GM-CSF revealed a delay in the accumulation of cells with dendritic cell features relative to controls; however, these cells were nearly as potent on a per cell basis as wild type cells in the stimulation of allogeneic mixed lymphocyte cultures. Similarly, skin Langerhans cells from mutant mice also showed significant ability to stimulate allogeneic T cells in culture. Since these findings cannot explain the defect in immune responses and the absence of secondary lymphoid tissues, we also looked at the ability of the relB mutant dendritic-like cells to form aggregates in vitro with naive syngeneic T cells. In this case, while wild type dendritic cells generated compact aggregates with T cells, relB mutant cells only formed irregular small aggregates. Thus, while relB mutant dendritic-like cells have some functions of mature dendritic cells, other functions are deficient. Understanding the role of relB in regulation of these functions should lead to a greater understanding of the molecular basis of dendritic cell development and function.

Keywords

Dendritic Cell Bone Marrow Culture Mature Dendritic Cell Scripps Research Institute Dendritic Cell Function 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1997

Authors and Affiliations

  • Lisa Dimolfetto
    • 1
  • Christina Reilly
    • 1
  • Qun Wei
    • 1
  • David Lo
    • 1
  1. 1.Department of Immunology IMM-25The Scripps Research InstituteLa JollaUSA

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