Identification of a Borrelia burgdorferi OspA T Cell Epitope That Promotes Anti-OspA IgG in Mice

Linda K. Bockenstedt, Erol Fikrig, Stephen W Barthold, Richard A. Flavell, Fred S. Kantor

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

Lyme disease, due to infection with the tick-borne spirochete Borrelia burgdorferi, is a multisystem disorder that can lead to chronic disabling symptoms. Abs to the outer surface protein A (OspA) of B. burgdorferi provide protection against infection, and OspA is now the basis of a first generation recombinant vaccine undergoing phase III efficacy studies. Recent studies have suggested that T cells reactive with N-terminal epitopes in OspA could contribute to the development of treatment-resistant Lyme arthritis. In the present studies, we use the murine model of Lyme borreliosis to define an OspA T cell epitope located in the carboxyl terminus that accelerates anti-OspA IgG production after infection. In addition, we show that this T cell epitope is elicited by immunization with rOspA or with a truncated form of OspA that contains the B cell epitope targeted by protective OspA mAb. Polyclonal antisera to the truncated OspA fragment can protect mice from challenge infection. These results are the first demonstration of a B. burgdorferi-specific peptide that elicits a biologically important T cell response in vivo and have implications for the design of a second generation OspA-based subunit vaccine.

Original languageEnglish (US)
Pages (from-to)5496-5502
Number of pages7
JournalJournal of Immunology
Volume157
Issue number12
StatePublished - Dec 15 1996
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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    Bockenstedt, L. K., Fikrig, E., Barthold, S. W., Flavell, R. A., & Kantor, F. S. (1996). Identification of a Borrelia burgdorferi OspA T Cell Epitope That Promotes Anti-OspA IgG in Mice. Journal of Immunology, 157(12), 5496-5502.