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The Bruton tyrosine kinase inhibitor PCI-32765 ameliorates autoimmune arthritis by inhibition of multiple effector cells

Betty Y Chang1*, Min Mei Huang1, Michelle Francesco1, Jun Chen1, Jeremy Sokolove23, Padmaja Magadala1, William H Robinson23 and Joseph J Buggy1

Author Affiliations

1 Pharmacyclics, Inc., Research Department, Sunnyvale CA, 94085-4521, USA

2 Stanford University School of Medicine, Division of Immunology and Rheumatology, Stanford, CA. 94305

3 VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, CA, 94304, USA

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Arthritis Research & Therapy 2011, 13:R115  doi:10.1186/ar3400

Published: 13 July 2011

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Additional file 1:

Table S1. Immunophenotyping of splenocyte subpopulations following 18 days of treatment with PCI-32765.

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Additional file 2:

Figure S1. Serum cytokines/chemokines from collagen-induced arthritis (CIA) mice treated with PCI-32765 at 12.5 mg/kg (n = 12) for 18 days. * P < 0.05 compared with vehicle, analysis of variance.

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Additional file 3:

Supplementary materials and methods. Immunophenotyping of mouse spleens from collagen-induced arthritis (CIA) models.

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Additional file 4:

Figure S2. PCI-32765 potentially inhibits multiple pathways in the pathogenesis of rheumatoid arthritis. PCI-32765 inhibits B cell activation, and suppresses cytokine/chemokine production from monocytes, macrophages, and mast cells following immune-complex activation (modified from [49]). Art by Jacqueline Schaffer, M.A.M.S., medical illustrator, for Pharmacyclics Inc.

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