原创力文档the bruton tyrosine kinase inhibitor pci-32765 ameliorates autoimmune arthritis by inhibition of multiple effector cells布鲁顿酪氨酸激酶抑制剂的pci - 32765改善自身免疫性关节炎多效应细胞的抑制作用.pdfVIP
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the bruton tyrosine kinase inhibitor pci-32765 ameliorates autoimmune arthritis by inhibition of multiple effector cells布鲁顿酪氨酸激酶抑制剂的pci - 32765改善自身免疫性关节炎多效应细胞的抑制作用
The Bruton tyrosine kinase inhibitor PCI-32765
ameliorates autoimmune arthritis by inhibition of
multiple effector cells
Chang et al.
Chang et al. Arthritis Research Therapy 2011, 13:R115
/content/13/4/R115 (13 July 2011)
Chang et al. Arthritis Research Therapy 2011, 13:R115
/content/13/4/R115
RESEARCH ARTICLE Open Access
The Bruton tyrosine kinase inhibitor PCI-32765
ameliorates autoimmune arthritis by inhibition of
multiple effector cells
1* 1 1 1 2,3 1
Betty Y Chang , Min Mei Huang , Michelle Francesco , Jun Chen , Jeremy Sokolove , Padmaja Magadala ,
William H Robinson2,3 and Joseph J Buggy1
Abstract
Introduction: The aim was to determine the effect of the Bruton tyrosine kinase (Btk)-selective inhibitor PCI-32765,
currently in Phase I/II studies in lymphoma trials, in arthritis and immune-complex (IC) based animal models and
describe the underlying cellular mechanisms.
Methods: PCI-32765 was administered in a series of murine IC disease models including collagen-induced arthritis
(CIA), collagen antibody-induced arthritis (CAIA), reversed passive anaphylactic reaction (RPA), and passive
cutaneous anaphylaxis (PCA). Clinical and pathologic features characteristic of each model were examined
following treatment. PCI-32765 was then examined in assays using immune cells relevant to the pathogenesis of
arthritis, and where Btk is thought to play a functional role. These included proliferation and calcium mobilization
in B cells, cytokine and chemokine production in monocytes/macrophages, degranulation of mast cells and its
subsequent cytokine/chemoki
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