Virus-specific, CD8(+) major histocompatibility complex class I-restricted cytotoxic T lymphocytes in lymphocytic choriomeningitis virus-infected beta(2)-microglobulin-deficient mice

Daniel Quinn, AJ Zajac, CE Hioe, JA Frelinger

    Research output: Contribution to journalArticle

    Abstract

    Following infection with lymphocytic choriomeningitis virus (LCMV), normal adult mice generate virus-specific, major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTL) which clear the virus after intraperitoneal infection or cause death following intracranial (i.c.) infection. We have investigated the response of beta(2)-microglobulin-deficient (beta(2)m(-)) mice of the H-2(d) haplotype (KOD mice) to LCMV infection. Unlike H-2(b) beta(2)m(-) mice, which generate CD4(+) MHC class II-restricted CTL in response to LCMV, KOD mice generate high levels of CD8(+) MHC class I-restricted, virus-specific CTL. These CTL are specific for the LCMV nucleoprotein epitope (residues 118 to 126) in association with the L-d class I molecule, analogous to the CTL response in wild-type mice. KOD mice are also susceptible to lethal LCM disease, with 75 to 80% of the mice dying 7 to 9 days following i.c. infection with virus. Similar to results with normal mice, lethal LCM disease in KOD mice is prevented by in vivo depletion of CD8(+) T cells prior to i.c. infection. In contrast to wild-type mice, however, KOD mice cannot control LCMV and become persistently infected. Overall, these results demonstrate that beta(2)m is not an absolute requirement for presentation of endogenous antigen on L-d or for induction of virus-specific L-d-restricted CTL in vivo.
    LanguageEnglish
    Pages8392-8396
    JournalJournal of Virology
    Volume71
    Issue number11
    Publication statusPublished - Nov 1997

    Fingerprint

    Lymphocytic choriomeningitis virus
    beta 2-Microglobulin
    Cytotoxic T-Lymphocytes
    Major Histocompatibility Complex
    Viruses
    Virus Diseases
    Infection
    Virus Activation
    Nucleoproteins
    Haplotypes
    Epitopes
    Cause of Death

    Cite this

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    title = "Virus-specific, CD8(+) major histocompatibility complex class I-restricted cytotoxic T lymphocytes in lymphocytic choriomeningitis virus-infected beta(2)-microglobulin-deficient mice",
    abstract = "Following infection with lymphocytic choriomeningitis virus (LCMV), normal adult mice generate virus-specific, major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTL) which clear the virus after intraperitoneal infection or cause death following intracranial (i.c.) infection. We have investigated the response of beta(2)-microglobulin-deficient (beta(2)m(-)) mice of the H-2(d) haplotype (KOD mice) to LCMV infection. Unlike H-2(b) beta(2)m(-) mice, which generate CD4(+) MHC class II-restricted CTL in response to LCMV, KOD mice generate high levels of CD8(+) MHC class I-restricted, virus-specific CTL. These CTL are specific for the LCMV nucleoprotein epitope (residues 118 to 126) in association with the L-d class I molecule, analogous to the CTL response in wild-type mice. KOD mice are also susceptible to lethal LCM disease, with 75 to 80{\%} of the mice dying 7 to 9 days following i.c. infection with virus. Similar to results with normal mice, lethal LCM disease in KOD mice is prevented by in vivo depletion of CD8(+) T cells prior to i.c. infection. In contrast to wild-type mice, however, KOD mice cannot control LCMV and become persistently infected. Overall, these results demonstrate that beta(2)m is not an absolute requirement for presentation of endogenous antigen on L-d or for induction of virus-specific L-d-restricted CTL in vivo.",
    author = "Daniel Quinn and AJ Zajac and CE Hioe and JA Frelinger",
    year = "1997",
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    pages = "8392--8396",
    journal = "Journal of Virology",
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    Virus-specific, CD8(+) major histocompatibility complex class I-restricted cytotoxic T lymphocytes in lymphocytic choriomeningitis virus-infected beta(2)-microglobulin-deficient mice. / Quinn, Daniel; Zajac, AJ; Hioe, CE; Frelinger, JA.

    In: Journal of Virology, Vol. 71, No. 11, 11.1997, p. 8392-8396.

    Research output: Contribution to journalArticle

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    N2 - Following infection with lymphocytic choriomeningitis virus (LCMV), normal adult mice generate virus-specific, major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTL) which clear the virus after intraperitoneal infection or cause death following intracranial (i.c.) infection. We have investigated the response of beta(2)-microglobulin-deficient (beta(2)m(-)) mice of the H-2(d) haplotype (KOD mice) to LCMV infection. Unlike H-2(b) beta(2)m(-) mice, which generate CD4(+) MHC class II-restricted CTL in response to LCMV, KOD mice generate high levels of CD8(+) MHC class I-restricted, virus-specific CTL. These CTL are specific for the LCMV nucleoprotein epitope (residues 118 to 126) in association with the L-d class I molecule, analogous to the CTL response in wild-type mice. KOD mice are also susceptible to lethal LCM disease, with 75 to 80% of the mice dying 7 to 9 days following i.c. infection with virus. Similar to results with normal mice, lethal LCM disease in KOD mice is prevented by in vivo depletion of CD8(+) T cells prior to i.c. infection. In contrast to wild-type mice, however, KOD mice cannot control LCMV and become persistently infected. Overall, these results demonstrate that beta(2)m is not an absolute requirement for presentation of endogenous antigen on L-d or for induction of virus-specific L-d-restricted CTL in vivo.

    AB - Following infection with lymphocytic choriomeningitis virus (LCMV), normal adult mice generate virus-specific, major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTL) which clear the virus after intraperitoneal infection or cause death following intracranial (i.c.) infection. We have investigated the response of beta(2)-microglobulin-deficient (beta(2)m(-)) mice of the H-2(d) haplotype (KOD mice) to LCMV infection. Unlike H-2(b) beta(2)m(-) mice, which generate CD4(+) MHC class II-restricted CTL in response to LCMV, KOD mice generate high levels of CD8(+) MHC class I-restricted, virus-specific CTL. These CTL are specific for the LCMV nucleoprotein epitope (residues 118 to 126) in association with the L-d class I molecule, analogous to the CTL response in wild-type mice. KOD mice are also susceptible to lethal LCM disease, with 75 to 80% of the mice dying 7 to 9 days following i.c. infection with virus. Similar to results with normal mice, lethal LCM disease in KOD mice is prevented by in vivo depletion of CD8(+) T cells prior to i.c. infection. In contrast to wild-type mice, however, KOD mice cannot control LCMV and become persistently infected. Overall, these results demonstrate that beta(2)m is not an absolute requirement for presentation of endogenous antigen on L-d or for induction of virus-specific L-d-restricted CTL in vivo.

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