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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.

Original publication




Journal article


Cell Immunol

Publication Date





184 - 192


Animals, Antibodies, Viral, Antigens, Viral, B-Lymphocytes, CD40 Antigens, Complement C3, Elapid Venoms, Immunization, Immunoglobulin M, Killer Cells, Natural, Lymphocyte Activation, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Nucleopolyhedrovirus, Receptors, Tumor Necrosis Factor, Recombinant Fusion Proteins, Signal Transduction, T-Lymphocytes, Helper-Inducer, Vesicular stomatitis Indiana virus, Viral Envelope Proteins, Viral Vaccines