Protective antibodies in murine Lyme disease arise independently of CD40 ligand

Erol Fikrig, Stephen W Barthold, Manchuan Chen, Iqbal S. Grewal, Joe Craft, Richard A. Flavell

Research output: Contribution to journalArticle

53 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1-3
Number of pages3
JournalJournal of Immunology
Volume157
Issue number1
StatePublished - Jul 1 1996
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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    Fikrig, E., Barthold, S. W., Chen, M., Grewal, I. S., Craft, J., & Flavell, R. A. (1996). Protective antibodies in murine Lyme disease arise independently of CD40 ligand. Journal of Immunology, 157(1), 1-3.