Research article
The Bruton tyrosine kinase inhibitor PCI-32765 ameliorates autoimmune arthritis by inhibition of multiple effector cells
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
Arthritis Research & Therapy 2011, 13:R115 doi:10.1186/ar3400
Published: 13 July 2011Additional files
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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