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Related Experiment Videos

Variable immune response against a developmentally regulated self-antigen.

U Steinhoff1, K J Maloy, C Burkhart

  • 1Department of Immunology, Max-Planck Institute for Infection Biology, Monbijoustrasse 2, Berlin, D-10117, Germany. steinhoff@mplib-berlin.mpg.de

Journal of Autoimmunity
|February 24, 1999
PubMed
Summary

Transgenic mice expressing vesicular stomatitis virus glycoprotein (VSV-G) showed impaired T helper cell responses, suggesting clonal deletion and peripheral anergy regulate immune responses to VSV-G.

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Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • Vesicular stomatitis virus glycoprotein (VSV-G) is a key viral antigen.
  • Transgenic mouse models are crucial for studying immune responses.
  • Understanding T and B cell reactivity is vital for vaccine development.

Purpose of the Study:

  • To investigate T and B cell reactivity against VSV-G in transgenic mice.
  • To elucidate the mechanisms regulating immune responses to VSV-G.
  • To analyze the impact of age on immune cell activity.

Main Methods:

  • Generation of transgenic mice expressing VSV-G under a hormone-regulated promoter.
  • Immunization with recombinant vaccinia virus expressing VSV-G.
  • Analysis of T helper cell activity and B cell responses (IgM, IgG).

Related Experiment Videos

  • Assessment of T cell receptor (TCR) transgenic CD4(+) T cells.

    • Main Results:

    • VSV-G expression varied with age in the thymus.
    • Normal VSV-G-specific IgM but reduced IgG responses were observed.
    • T helper cell activity was impaired early and late in life.
    • TCR transgenic CD4(+) T cells showed early deletion followed by peripheral repopulation.

    Conclusions:

    • Two distinct mechanisms regulate immune responses to VSV-G: early clonal deletion and later peripheral anergy.
    • Age-dependent regulation of immune responses is evident.
    • Findings provide insights into tolerance induction and immune regulation.