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Possible mechanisms by which the H-2Kbm3 mutation may decrease cytotoxic T-lymphocyte recognition of vesicular

M R Bowman, D S Lyles, J W Parce

    Journal of Virology
    |June 1, 1987
    PubMed
    Summary

    Mice with a mutated H-2Kb molecule show a weaker cytotoxic T-lymphocyte (CTL) response to vesicular stomatitis virus (VSV). This impaired immune response is due to inefficient target cell recognition and reduced effector cell generation, impacting viral clearance.

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    Area of Science:

    • Immunology
    • Virology
    • Molecular Biology

    Background:

    • Cytotoxic T-lymphocytes (CTLs) are crucial for antiviral immunity.
    • Vesicular stomatitis virus (VSV) is a model pathogen for studying CTL responses.
    • The H-2Kb molecule plays a role in antigen presentation to CTLs.

    Purpose of the Study:

    • To investigate the impact of a mutation in the H-2Kb molecule on anti-VSV CTL responses in mice.
    • To elucidate the mechanisms underlying the altered CTL activity in H-2bm3 mice.

    Main Methods:

    • Generation and characterization of anti-VSV CTL responses in C57BL/6 (B6) and B6-H-2bm3 (bm3) mice.
    • Use of recombinant vaccinia viruses to identify VSV-specific CTL targets.
    • Assessment of target cell recognition and lysis using various cell lines and primary cells.

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  • Analysis of H-2Kb-restricted and H-2Db-restricted CTL activity.
  • Radiolabeling and immunoprecipitation to compare viral antigen and H-2K expression.

    • Main Results:

    • Spleen cells from bm3 mice required a 10-fold higher dose of VSV to generate secondary anti-VSV CTL compared to B6 mice.
    • Anti-VSV CTL in both mouse strains primarily recognized the VSV nucleocapsid (N) protein.
    • bm3 CTL exhibited significantly lower lytic activity against VSV-infected autologous cells and H-2b tumor cell lines.
    • Inefficient recognition of VSV-infected bm3 target cells by both bm3 and B6 CTL was observed.
    • H-2Kb-restricted CTL responses were significantly lower in bm3 mice, while H-2Db-restricted responses were similar.
    • VSV-infected B6 and bm3 cells expressed equivalent levels of viral antigens and H-2K.

    Conclusions:

    • The mutation in the H-2Kb molecule of bm3 mice impairs the recognition of VSV-infected cells.
    • This impairment is a major cause of the reduced anti-VSV CTL response in bm3 mice.
    • The bm3 mutation likely alters a functional site on H-2Kb, reducing its affinity for viral antigen or CTL receptors, thereby affecting antiviral immunity.