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The humoral immune response to Borrelia burgdorferi during persistent infection is critical to both protective and
disease-resolving immunity. This study examined the role of B cells in the absence of T cells during these events, using mice with selected immune dysfunctions. At 6 weeks postinfection, an interval at which arthritis resolves in immunocompetent mice, arthritis severity was equivalent among immunocompetent mice, alphabeta(+)-T-cell-deficient mice, and mice lacking both alphabeta(+) and gammadelta(+) T cells. Arthritis severity was worse in SCID mice, which lack T and B lymphocytes. Carditis regressed in immunocompetent mice and those lacking both alphabeta(+) and gammadelta(+) T cells but remained active in mice lacking only alphabeta(+) T cells and in SCID mice. Mice lacking only alphabeta(+) T cells and those lacking both alphabeta(+) and gammadelta(+) T cells generated immunoglobulin M (IgM) and IgG3 B. burgdorferi-reactive antibodies. Sera from infected immunocompetent mice, mice lacking only alphabeta(+) T cells, and mice lacking both alphabeta(+) and gammadelta(+) T cells passively protected naive mice against challenge inoculation with B. burgdorferi. However, only sera from infected immunocompetent mice, but not sera from infected T-cell-deficient mice, were able to resolve arthritis when passively transferred to actively infected SCID mice. These data demonstrate that B-cell activation during a T-cell-independent response may be critical for resolution of arthritis and carditis and that protective antibodies are generated during this response.