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Related Experiment Videos

A role for immunoglobulin D: interference with tolerance induction

R Carsetti1, G Köhler, M C Lamers

  • 1Max-Planck-Institute for Immunobiology, Freiburg, FRG.

European Journal of Immunology
|January 1, 1993
PubMed
Summary
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Antigen-mediated B cell tolerance induction involves B lymphocyte apoptosis. Surface IgD (sIgD) interferes with this process, protecting B cells from deletion and enabling immune responses.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • B lymphocyte tolerance is crucial for preventing autoimmunity.
  • Immune tolerance mechanisms in B cells are complex and involve multiple signaling pathways.
  • Understanding B cell tolerance induction is key to developing therapies for autoimmune diseases.

Purpose of the Study:

  • To investigate the role of surface IgM (sIgM) and surface IgD (sIgD) in B lymphocyte tolerance induction.
  • To identify the specific B cell developmental stage sensitive to tolerance induction.
  • To determine the functional capacity of B cells surviving tolerance induction.

Main Methods:

  • Transgenic mice expressing sIgM or sIgM and sIgD were treated with TNP-modified antigens.
  • B cell populations were analyzed for deletion and apoptosis.

Related Experiment Videos

  • Cell surface markers were used to characterize B cell developmental stages.
  • Intracellular calcium ([Ca2+]i) levels were measured to assess B cell function.

    • Main Results:

    • Antigen-mediated cross-linking of sIgM induced B cell deletion via apoptosis in both neonatal and adult mice.
    • The presence of sIgD hindered tolerance induction.
    • B cells sensitive to deletion were in a transitional stage between immature and mature phenotypes.
    • Surviving B cells remained functional, exhibiting normal calcium signaling.

    Conclusions:

    • sIgM signaling mediates B cell deletion in the absence of T cell help during late maturation stages.
    • sIgD expression protects B cells from deletion, allowing them to participate in immune responses.
    • These findings elucidate critical mechanisms of B cell tolerance and self-reactivity screening.