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Repeated influenza virus infection induces the production of dominantly IgG2a-type virus-specific antibodies as well as the appearance of IgG2a-reactive autoantibodies in BALB/c mice characterized by low spontaneous rheumatoid factor-type autoantibody production. IgG2a-reactive autoantibody-producing hybridomas could be isolated from the spleen of influenza virus-infected BALB/c mice. The mAb produced by these clones represent not only IgM but also IgG and IgA isotypes and show strong isotype or isoallotype specificity. The common functional property of these autoantibodies is their preferential- and high-affinity binding to complexed, solid-phase-bound or heat-aggregated IgG2a when compared to native soluble or cell-bound IgG2a. The mechanism of induction and the possible biological function of these autoantibodies are discussed in the light of their fine specificity and functional properties.
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