Protective antibodies in murine Lyme disease arise independently of CD40 ligand.
Open Access
- 1 July 1996
- journal article
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 157 (1) , 1-3
- https://doi.org/10.4049/jimmunol.157.1.1
Abstract
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.Keywords
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