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The Journal of Immunology, Vol 157, Issue 1 1-3, Copyright © 1996 by American Association of Immunologists
CUTTING EDGE |
E Fikrig, SW Barthold, M Chen, IS Grewal, J Craft and RA Flavell
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Borrelia burgdorferi-infected mice develop acute arthritis that undergoes Ab-mediated resolution. To further investigate the role of B. burgdorferi-specific Abs in Lyme borreliosis, CD40 ligand-deficient (CD40L-deficient) mice were infected with B. burgdorferi. The development and regression of arthritis were similar in CD40L-deficient and control mice. Although CD40L-deficient mice have defects in Ig class switching, infected CD40L-deficient mice developed B. burgdorferi- specific IgG2b Abs. Moreover, the transfer of serum from B. burgdorferi- infected CD40L-deficient animals prevented infection in severe combined immunodeficient mice. These data show that B. burgdorferi-infected CD40L-deficient mice are capable of producing Abs that are protective, despite the inability of these mice to mediate T-dependent immune responses.
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