Comparison of CpG s-ODNs, chromatin immune complexes, and dsDNA fragment immune complexes in the TLR9-dependent activation of rheumatoid factor B cells

Author:

Marshak-Rothstein Ann1,Busconi Liliana2,Lau Christina M.2,Tabor Abigail S.2,Leadbetter Elizabeth A.3,Akira Shizuo4,Krieg Arthur M.5,Lipford Grayson B.5,Viglianti Gregory A.2,Rifkin Ian R.6

Affiliation:

1. Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA,

2. Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA

3. Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA

4. Research Institute for Microbial Diseases, Osaka University, Osaka, Japan

5. Coley Pharmaceutical Group, Wellesley, Massachusetts, USA

6. Renal Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA

Abstract

Synthetic single-stranded oligodeoxynucleotides (15—30 bp) containing CpG motifs and phosphorothioate backbones (CpG s-ODN), immune complexes consisting of anti-nucleosome mAbs and mammalian chromatin (chromatin IC), and immune complexes consisting of anti-hapten mAbs and haptenated-double stranded DNA fragments (~600 bp) can all effectively stimulate transgenic B cells expressing a rheumatoid factor receptor by a TLR9-dependent process. However, differential sensitivity to both s-ODN and small molecule inhibitors suggests that stimulatory CpG sODN and chromatin IC may either access TLR9 via different routes or depend on discrete activation parameters. These data have important implications regarding the therapeutic application of TLR9 inhibitors to the treatment of systemic autoimmune diseases.

Publisher

SAGE Publications

Subject

Infectious Diseases,Cell Biology,Molecular Biology,Immunology,Microbiology

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