Immunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.

Mice rendered B cell deficient by targeted disruption of the immunoglobulin mu chain gene (IgM-/- mice) were used to analyze the role of antibodies and B cells in viral infections; homozygous IgM-/- mice were bred in a way to avoid transmission of maternal antibodies. After infection with vesicular...

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Main Authors: Bründler, M, Aichele, P, Bachmann, M, Kitamura, D, Rajewsky, K, Zinkernagel, R
Format: Journal article
Jezik:English
Izdano: 1996
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author Bründler, M
Aichele, P
Bachmann, M
Kitamura, D
Rajewsky, K
Zinkernagel, R
author_facet Bründler, M
Aichele, P
Bachmann, M
Kitamura, D
Rajewsky, K
Zinkernagel, R
author_sort Bründler, M
collection OXFORD
description Mice rendered B cell deficient by targeted disruption of the immunoglobulin mu chain gene (IgM-/- mice) were used to analyze the role of antibodies and B cells in viral infections; homozygous IgM-/- mice were bred in a way to avoid transmission of maternal antibodies. After infection with vesicular stomatitis virus (VSV), IgM-/- mice developed paralytic disease and subsequently died, whereas C57BL/6 control mice or IgM-/- mice passively protected with VSV-neutralizing antibodies survived. Furthermore, IgM-/- mice showed increased natural killer (NK) activity upon exposure to either lymphocytic choriomeningitis virus (LCMV) or to poly(I).poly(C), while NK activity in untreated IgM-/- mice was within normal ranges. Cytotoxic T cell responses were comparable in IgM-/- and control mice infected either with VSV or with vaccinia virus or with low doses of LCMV (10(2) infectious focus-forming units [ifu]). After intracerebral infection with LCMV-Armstrong, CD8+ T cell-mediated lethal lymphocytic choriomeningitis developed independently of the presence of B cells and antibodies. After infection with high doses (2 x 10(6) - 5 x 10(6) ifu) of LCMV-WE or LCMV-Docile, IgM-/- mice exhibited a reduced capacity to control these primary infections and had elevated virus titers for prolonged times (> 60 days). Nevertheless, the cytotoxic T cell response against LCMV in the early phase of infection was comparable in IgM-/- and control mice, but disappeared in those IgM-/- mice which had a persistent viral infection. Cytotoxic T cell memory was apparently unimpaired in low-dose-primed IgM-/- mice, which were able to control the primary virus infection; both IgM-/- and control mice cleared a high intravenous dose of virus within 2 days after challenge infection. This indicates that an efficient T cell memory against LCMV was established in the absence of B cells.
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spelling oxford-uuid:b4eb67bd-1ceb-439b-8300-7630c39c96c62022-03-27T04:29:33ZImmunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:b4eb67bd-1ceb-439b-8300-7630c39c96c6EnglishSymplectic Elements at Oxford1996Bründler, MAichele, PBachmann, MKitamura, DRajewsky, KZinkernagel, RMice rendered B cell deficient by targeted disruption of the immunoglobulin mu chain gene (IgM-/- mice) were used to analyze the role of antibodies and B cells in viral infections; homozygous IgM-/- mice were bred in a way to avoid transmission of maternal antibodies. After infection with vesicular stomatitis virus (VSV), IgM-/- mice developed paralytic disease and subsequently died, whereas C57BL/6 control mice or IgM-/- mice passively protected with VSV-neutralizing antibodies survived. Furthermore, IgM-/- mice showed increased natural killer (NK) activity upon exposure to either lymphocytic choriomeningitis virus (LCMV) or to poly(I).poly(C), while NK activity in untreated IgM-/- mice was within normal ranges. Cytotoxic T cell responses were comparable in IgM-/- and control mice infected either with VSV or with vaccinia virus or with low doses of LCMV (10(2) infectious focus-forming units [ifu]). After intracerebral infection with LCMV-Armstrong, CD8+ T cell-mediated lethal lymphocytic choriomeningitis developed independently of the presence of B cells and antibodies. After infection with high doses (2 x 10(6) - 5 x 10(6) ifu) of LCMV-WE or LCMV-Docile, IgM-/- mice exhibited a reduced capacity to control these primary infections and had elevated virus titers for prolonged times (> 60 days). Nevertheless, the cytotoxic T cell response against LCMV in the early phase of infection was comparable in IgM-/- and control mice, but disappeared in those IgM-/- mice which had a persistent viral infection. Cytotoxic T cell memory was apparently unimpaired in low-dose-primed IgM-/- mice, which were able to control the primary virus infection; both IgM-/- and control mice cleared a high intravenous dose of virus within 2 days after challenge infection. This indicates that an efficient T cell memory against LCMV was established in the absence of B cells.
spellingShingle Bründler, M
Aichele, P
Bachmann, M
Kitamura, D
Rajewsky, K
Zinkernagel, R
Immunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.
title Immunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.
title_full Immunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.
title_fullStr Immunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.
title_full_unstemmed Immunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.
title_short Immunity to viruses in B cell-deficient mice: influence of antibodies on virus persistence and on T cell memory.
title_sort immunity to viruses in b cell deficient mice influence of antibodies on virus persistence and on t cell memory
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