Human parvovirus B19 transgenic mice become susceptible to polyarthritis

Naruhiko Takasawa, Yasuhiko Munakata, Keiko Kumura Ishii, Yuichi Takahashi, Minako Takahashi, Yi Fu, Tomonori Ishii, Hiroshi Fujii, Takako Saito, Hiroshi Takano, Tetsuo Noda, Misao Suzuki, Masato Nose, Suzan Zolla-Patzner, Takeshi Sasaki

Research output: Contribution to journalArticlepeer-review

33 Citations (Scopus)

Abstract

Human parvovirus B19 (B19) often causes acute polyarthritis in adults. In this paper, we analyzed nucleotide sequences of the B19 genome of patients with rheumatoid arthritis (RA), and then introduced the monstructual protein 1 (NS1) gene of B19 into C57BL/6 mice that had a genetic origin not susceptible to arthritis. The transgenic mice developed no lesions spontaneously, but were susceptible to type II collagen (CII)-induced arthritis. B19 NS1 was expressed in synovial cells on the articular lesions that were histologically characteristic of granulomatous synovitis and pannus formation in cartilage and bone. Serum levels of anti-CII Abs and TNF-α increased in NS1 transgenic mice to the same levels as those of DBA/1 mice, which were susceptible to polyarthritis. Stimulation with CII increased secretion of Th1-type- and Th2-type cytokines in NS1 transgenic mice, indicating that a nonpermissive H-2b haplotype in the wild type of C57BL/6 mice can be made susceptible to polyarthritis through the expression of NS1. This study is the first to show that a viral agent from the joints in humans can cause CII-induced arthritis resembling RA.

Original languageEnglish
Pages (from-to)4675-4683
Number of pages9
JournalJournal of Immunology
Volume173
Issue number7
DOIs
Publication statusPublished - 2004 Oct 1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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