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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Format: | Journal article |
Jezik: | English |
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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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format | Journal article |
id | oxford-uuid:b4eb67bd-1ceb-439b-8300-7630c39c96c6 |
institution | University of Oxford |
language | English |
last_indexed | 2024-03-07T03:13:13Z |
publishDate | 1996 |
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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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