T-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal.
Vesicular stomatitis virus (VSV) induces a T helper cell-independent IgM antibody response, whereas the IgG response is strictly T helper cell dependent. Since VSV induces B cells in complete absence of T helper cells, the question arises as to whether this induction occurs in the absence of a secon...
| Main Authors: | , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
1996
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| _version_ | 1797056774805651456 |
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| author | Fehr, T Bachmann, M Bluethmann, H Kikutani, H Hengartner, H Zinkernagel, R |
| author_facet | Fehr, T Bachmann, M Bluethmann, H Kikutani, H Hengartner, H Zinkernagel, R |
| author_sort | Fehr, T |
| collection | OXFORD |
| description | Vesicular stomatitis virus (VSV) induces a T helper cell-independent IgM antibody response, whereas the IgG response is strictly T helper cell dependent. Since VSV induces B cells in complete absence of T helper cells, the question arises as to whether this induction occurs in the absence of a second signal or whether it depends upon an alternative or replacing signal 2. We therefore asked whether VSV has polyclonal B cell stimulator activity and/or whether B cell induction by VSV needs costimulation via complement or tumor necrosis factor (TNF) receptor or by natural killer (NK) cell activity. In vitro B cell proliferation assays and analysis of the in vivo antibody response in CD40-deficient mice excluded that VSV has properties of a polyclonal B cell stimulator. C3 depletion by cobra venom factor and application of anti-complement receptor antibodies showed that the T-independent IgM response was largely C3-independent except under very limiting antigen doses. Immunization of TNF receptor-deficient mice showed a normal anti-VSV IgM response, and in a cytotoxicity assay on YAC target cells there was no evidence of NK cell activation by VSV. Thus, VSV seems to induce B cells without polyclonal activation and/or C3, TNF, or NK cells functioning as a replacing second signal. |
| first_indexed | 2024-03-06T19:27:14Z |
| format | Journal article |
| id | oxford-uuid:1c2d0c0c-fb10-43df-888f-8f9bda6b3145 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T19:27:14Z |
| publishDate | 1996 |
| record_format | dspace |
| spelling | oxford-uuid:1c2d0c0c-fb10-43df-888f-8f9bda6b31452022-03-26T11:04:19ZT-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:1c2d0c0c-fb10-43df-888f-8f9bda6b3145EnglishSymplectic Elements at Oxford1996Fehr, TBachmann, MBluethmann, HKikutani, HHengartner, HZinkernagel, RVesicular stomatitis virus (VSV) induces a T helper cell-independent IgM antibody response, whereas the IgG response is strictly T helper cell dependent. Since VSV induces B cells in complete absence of T helper cells, the question arises as to whether this induction occurs in the absence of a second signal or whether it depends upon an alternative or replacing signal 2. We therefore asked whether VSV has polyclonal B cell stimulator activity and/or whether B cell induction by VSV needs costimulation via complement or tumor necrosis factor (TNF) receptor or by natural killer (NK) cell activity. In vitro B cell proliferation assays and analysis of the in vivo antibody response in CD40-deficient mice excluded that VSV has properties of a polyclonal B cell stimulator. C3 depletion by cobra venom factor and application of anti-complement receptor antibodies showed that the T-independent IgM response was largely C3-independent except under very limiting antigen doses. Immunization of TNF receptor-deficient mice showed a normal anti-VSV IgM response, and in a cytotoxicity assay on YAC target cells there was no evidence of NK cell activation by VSV. Thus, VSV seems to induce B cells without polyclonal activation and/or C3, TNF, or NK cells functioning as a replacing second signal. |
| spellingShingle | Fehr, T Bachmann, M Bluethmann, H Kikutani, H Hengartner, H Zinkernagel, R T-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal. |
| title | T-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal. |
| title_full | T-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal. |
| title_fullStr | T-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal. |
| title_full_unstemmed | T-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal. |
| title_short | T-independent activation of B cells by vesicular stomatitis virus: no evidence for the need of a second signal. |
| title_sort | t independent activation of b cells by vesicular stomatitis virus no evidence for the need of a second signal |
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