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Infection and Immunity, September 2000, p. 5190-5197, Vol. 68, No. 9
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

T-Cell-Independent Responses to Borrelia burgdorferi Are Critical for Protective Immunity and Resolution of Lyme Disease

Maureen D. McKisic* and Stephen W. Barthold

Center for Comparative Medicine, University of California, Davis, California 95616

Received 3 December 1999/Returned for modification 10 February 2000/Accepted 9 June 2000

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, alpha beta +-T-cell-deficient mice, and mice lacking both alpha beta + and gamma delta + T cells. Arthritis severity was worse in SCID mice, which lack T and B lymphocytes. Carditis regressed in immunocompetent mice and those lacking both alpha beta + and gamma delta + T cells but remained active in mice lacking only alpha beta + T cells and in SCID mice. Mice lacking only alpha beta + T cells and those lacking both alpha beta + and gamma delta + T cells generated immunoglobulin M (IgM) and IgG3 B. burgdorferi-reactive antibodies. Sera from infected immunocompetent mice, mice lacking only alpha beta + T cells, and mice lacking both alpha beta + and gamma delta + 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.

* Corresponding author. Mailing address: Center for Comparative Medicine, University of California, One Shields Ave., Davis, CA 95616. Phone: (530) 754-5496. Fax: (530) 752-7914. E-mail: mdmckisic{at}ucdavis.edu.

Infection and Immunity, September 2000, p. 5190-5197, Vol. 68, No. 9
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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