Journal
INFECTION AND IMMUNITY
Volume 68, Issue 9, Pages 5190-5197Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.68.9.5190-5197.2000
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Funding
- NIAID NIH HHS [R01 AI026815, AI-26815, AI-45253] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI026815, N01AI045253] Funding Source: NIH RePORTER
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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,lan 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.
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