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  • Oral presentation
  • Open Access

Postnatal Syk deletion in mice clarifies the function of Syk in an anti-collagen antibody-induced arthritis model

  • 1, 2,
  • 2,
  • 1 and
  • 1
Arthritis Research & Therapy201214 (Suppl 1) :O22

  • Published:


  • Rheumatoid Arthritis
  • Arthritis
  • Tyrosine Kinase
  • Disease Development
  • Cytoplasmic Protein
Spleen tyrosine kinase (Syk) is a cytoplasmic protein expressed mainly in immune cells including macrophages and neutrophils and is associated with receptors containing an immunoreceptor tyrosine-based activation motif (ITAM), such as Fcγ receptors. As Syk-mediated signaling plays an important role in activation of immune responses, to investigate whether specific interruption of Syk-mediated signaling can affect the development of rheumatoid arthritis (RA), we used tamoxifen-induced conditional Syk-KO mice (iSyk KO) to evaluate the importance of Syk on disease development. Using a collagen antibody-induced arthritis model (CAIA), iSyk KO mice showed significantly attenuated disease severity compared to Syk non-deleted mice (Figure 1). Although iSyk KO mice contained reduced B cell numbers after deletion of Syk in adulthood, B cells are not required for arthritis development in CAIA, as demonstrated by using muMT mice which lack B cells. On the other hand, Syk-deficient macrophages produced less MCP-1 and IL-6 than Syk-sufficient cells after FcR ligation, which can account for the absence of a pronounced accumulation of neutrophils and macrophages in the joints of iSyk KO mice. Our results demonstrate that Syk in macrophages is likely a key player in antibody-induced arthritis, mediating the release of pro-inflammatory cytokines and chemokines after macrophages bind anti-collagen antibody, and indicate that Syk is a promising target for arthritis therapy.
Figure 1
Figure 1

Arthritis development in iSyk KO mice. Arthritis was induced by i.p. administration of anti-collagen Ab followed by LPS. Arthritis score was monitored. *; P < 0.001, **; P < 0.01.

Authors’ Affiliations

Division of Molecular and Cellular Immunoscience, Department of Biomolecular Sciences, Faculty of Medicine, Saga University, Nabeshima Saga, 849-8501, Japan
Department of Molecular & Cellular Biology, Kobe Pharma Research Institute, Nippon Boehringer Ingelheim Co Ltd, Minatojima-Minamimachi, Chuo-ku, Kobe Hyogo, 650-0047, Japan


© Ozaki et al.; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.