Anti-p19 antibody treatment exacerbates lyme arthritis and enhances borreliacidal activity

Sara Heil Peterson, Dean T. Nardelli, Thomas F. Warner, Steven M. Callister, Jose R. Torrealba, Ronald F. Schell

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Considerable effort has been made to elucidate the mechanism of Lyme arthritis. We focused on p19, a cell cycle-regulating molecule, because it is known to inhibit cell cycle division of T lymphocytes which may be responsible for the induction of arthritis. We show that anti-p19 antibody treatment enhances the inflammatory response normally detected at the tibiotarsal joints of Borrelia burgdorferi-vaccinated and Borrelia bissettii challenged mice. Specifically, anti-p19 antibody treatment augmented the severity of inflammation within the synovial and subsynovial tissue. Moreover, treatment with anti-p19 antibody caused severe erosion of cartilage and bone with ankle joint destruction. In addition, anti-p19 antibody treatment of Borrelia-vaccinated and -challenged mice enhanced the borreliacidal antibody response, especially against the vaccine isolate. The novel activities of anti-p19 antibody show that p19 may be an important therapeutic site for the treatment of Lyme arthritis.

Original languageEnglish (US)
Pages (from-to)510-517
Number of pages8
JournalClinical and Vaccine Immunology
Volume14
Issue number5
DOIs
Publication statusPublished - May 2007

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ASJC Scopus subject areas

  • Clinical Biochemistry
  • Immunology
  • Immunology and Allergy
  • Microbiology (medical)

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