2011 Fiscal Year Final Research Report
ASC plays a role in the IL-1beta, IL-18 pathway of the immune response to type II collagen in collagen-induced arthritis
Project/Area Number |
21591939
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | Shinshu University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
TANIGUCHI Shunichiro 信州大学, 医学系研究科, 教授 (60117166)
EHARA Takashi 信州大学, 医学部, 准教授 (00203646)
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Co-Investigator(Renkei-kenkyūsha) |
KATO Hiroyuki 信州大学, 医学部, 教授 (40204490)
SAGARA Junji 信州大学, 医学部, 教授 (10225831)
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Research Collaborator |
YAMAZAKI Hideshi 信州大学, 医学系研究科, 大学院生
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Project Period (FY) |
2009 – 2011
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Keywords | リウマチ病学 / ASC |
Research Abstract |
We investigated the involvement of apoptosis-associated speck-like protein containing a caspase recruit domain(ASC) in the progression of murine collagen-induced arthritis(CIA) and collagen antibody-induced arthritis(CAIA) using ASC-deficient(ASC-/-) and wild-type(ASC+/+) mice. Analyses were performed by immunohistochemistry for tissues and ELISA for sera. We observed an increase in the expression of ASC, as well as IL-1β. and IL-18, in the joints of CIA DBA mice, which indicated that ASC is involved in disease development. Next, we demonstrated that the infiltration of inflammatory cells and cartilage/bone destruction in CIA knee joints were significantly increased in ASC+/+ mice compared with ASC-/-mice. No such differences were noted in ASC+/+ and ASC-/-CAIA mice. In terms of cytokine expression in knee joints, IL-1β. and IL-18 were depressed in ASC-deficient CIA mice compared with wild-type mice, but were similarly expressed in CAIA joints in both mice groups. Taken together, we can conclude that ASC is involved in the development of CIA and plays a role in the priming phase of the immune response to type II collagen.
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Research Products
(4 results)