CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response.
The ligand for CD40 (CD40L) is expressed on the surface of activated CD4+ T cells and its role in T-B cell collaborations and thymus-dependent humoral immunity is well established. Recently, by generating CD40L-knockout mice, we have confirmed its previously described role in humoral immunity and de...
| Main Authors: | , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
1996
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| _version_ | 1797092298989764608 |
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| author | Borrow, P Tishon, A Lee, S Xu, J Grewal, I Oldstone, M Flavell, R |
| author_facet | Borrow, P Tishon, A Lee, S Xu, J Grewal, I Oldstone, M Flavell, R |
| author_sort | Borrow, P |
| collection | OXFORD |
| description | The ligand for CD40 (CD40L) is expressed on the surface of activated CD4+ T cells and its role in T-B cell collaborations and thymus-dependent humoral immunity is well established. Recently, by generating CD40L-knockout mice, we have confirmed its previously described role in humoral immunity and defined another important function of this molecule in the in vivo clonal expansion of antigen-specific CD4+ T cells. Here, we investigated the potential in vivo role of CD40L in antiviral immunity by examining the immune response mounted by CD40L-deficient mice following infection with lymphocytic choriomeningitis virus (LCMV), Pichinde virus, or vesicular stomatitis virus. Humoral immune responses of CD40L-deficient mice to these viruses were severely compromised, although moderate titres of antiviral IgM and some IgG2a were produced by virus-infected CD40L-deficient mice by a CD4+ T cell-independent mechanism. By contrast, CD40L-deficient mice made strong primary CTL responses to all three viruses. Interestingly however, although memory CTL activity was detectable in CD40L-deficient mice two months after infection with LCMV, the memory CTL response was much less efficient than in wild-type mice. Together, the results show that CD40-CD40L interactions are required for strong antiviral humoral immune responses, and reveal a novel role for CD40L in the establishment and/or maintenance of CD8+ CTL memory. |
| first_indexed | 2024-03-07T03:44:11Z |
| format | Journal article |
| id | oxford-uuid:bee4e412-dc57-4946-8188-cb34c1c0fd19 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T03:44:11Z |
| publishDate | 1996 |
| record_format | dspace |
| spelling | oxford-uuid:bee4e412-dc57-4946-8188-cb34c1c0fd192022-03-27T05:43:24ZCD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:bee4e412-dc57-4946-8188-cb34c1c0fd19EnglishSymplectic Elements at Oxford1996Borrow, PTishon, ALee, SXu, JGrewal, IOldstone, MFlavell, RThe ligand for CD40 (CD40L) is expressed on the surface of activated CD4+ T cells and its role in T-B cell collaborations and thymus-dependent humoral immunity is well established. Recently, by generating CD40L-knockout mice, we have confirmed its previously described role in humoral immunity and defined another important function of this molecule in the in vivo clonal expansion of antigen-specific CD4+ T cells. Here, we investigated the potential in vivo role of CD40L in antiviral immunity by examining the immune response mounted by CD40L-deficient mice following infection with lymphocytic choriomeningitis virus (LCMV), Pichinde virus, or vesicular stomatitis virus. Humoral immune responses of CD40L-deficient mice to these viruses were severely compromised, although moderate titres of antiviral IgM and some IgG2a were produced by virus-infected CD40L-deficient mice by a CD4+ T cell-independent mechanism. By contrast, CD40L-deficient mice made strong primary CTL responses to all three viruses. Interestingly however, although memory CTL activity was detectable in CD40L-deficient mice two months after infection with LCMV, the memory CTL response was much less efficient than in wild-type mice. Together, the results show that CD40-CD40L interactions are required for strong antiviral humoral immune responses, and reveal a novel role for CD40L in the establishment and/or maintenance of CD8+ CTL memory. |
| spellingShingle | Borrow, P Tishon, A Lee, S Xu, J Grewal, I Oldstone, M Flavell, R CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response. |
| title | CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response. |
| title_full | CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response. |
| title_fullStr | CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response. |
| title_full_unstemmed | CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response. |
| title_short | CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response. |
| title_sort | cd40l deficient mice show deficits in antiviral immunity and have an impaired memory cd8 ctl response |
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