Host response to Sendai virus in mice lacking class II major histocompatibility complex glycoproteins.
about
Natural pathogens of laboratory mice, rats, and rabbits and their effects on research.Quantifying the early immune response and adaptive immune response kinetics in mice infected with influenza A virus.Memory CD4 T cells direct protective responses to influenza virus in the lungs through helper-independent mechanisms.Virus-specific CD8(+) T cell numbers are maintained during gamma-herpesvirus reactivation in CD4-deficient mice.Protection against lethal encephalomyocarditis virus infection in the absence of serum-neutralizing antibodies.Diminished primary and secondary influenza virus-specific CD8(+) T-cell responses in CD4-depleted Ig(-/-) mice.Roles of major histocompatibility complex class II in inducing protective immune responses to influenza vaccinationUpregulation of class I major histocompatibility complex antigens by interferon gamma is necessary for T-cell-mediated elimination of recombinant adenovirus-infected hepatocytes in vivoMHC class II-alpha chain knockout mice support increased viral replication that is independent of their lack of MHC class II cell surface expression and associated immune function deficiencies.Selection of a single amino acid substitution in the hemagglutinin molecule by chicken eggs can render influenza A virus (H3) candidate vaccine ineffectiveDifferential antigen burden modulates the gamma interferon but not the immunoglobulin response in mice that vary in susceptibility to Sendai virus pneumoniaImmune CD4+ T cells promote the clearance of influenza virus from major histocompatibility complex class II -/- respiratory epitheliumTheiler's virus persistence and demyelination in major histocompatibility complex class II-deficient miceDifferent roles for CD4+ and CD8+ T lymphocytes and macrophage subsets in the control of a generalized virus infection.Progressive loss of CD8+ T cell-mediated control of a gamma-herpesvirus in the absence of CD4+ T cells.CD40-independent pathways of T cell help for priming of CD8(+) cytotoxic T lymphocytes.Pathogenesis of an infectious mononucleosis-like disease induced by a murine gamma-herpesvirus: role for a viral superantigen?The cytotoxic T-lymphocyte response to Sendai virus is unimpaired in the absence of gamma interferon.Influence of CD4 T cells and the source of major histocompatibility complex class II-restricted peptides on cytotoxic T-cell priming by dendritic cells
P2860
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P2860
Host response to Sendai virus in mice lacking class II major histocompatibility complex glycoproteins.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
1995年论文
@zh
1995年论文
@zh-cn
name
Host response to Sendai virus ...... ibility complex glycoproteins.
@ast
Host response to Sendai virus ...... ibility complex glycoproteins.
@en
type
label
Host response to Sendai virus ...... ibility complex glycoproteins.
@ast
Host response to Sendai virus ...... ibility complex glycoproteins.
@en
prefLabel
Host response to Sendai virus ...... ibility complex glycoproteins.
@ast
Host response to Sendai virus ...... ibility complex glycoproteins.
@en
P2093
P2860
P1433
P1476
Host response to Sendai virus ...... tibility complex glycoproteins
@en
P2093
P2860
P304
P407
P577
1995-03-01T00:00:00Z