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ASC plays a role in the IL-1beta, IL-18 pathway of the immune response to type II collagen in collagen-induced arthritis

ASC plays a role in the IL-1beta, IL-18 pathway of the immune response to type II collagen in collagen-induced arthritis
ASC 在胶原诱导性关节炎中对 II 型胶原免疫反应的 IL-1beta、IL-18 通路中发挥作用
批准号:
21591939
负责人:
TAKEOKA Michiko
金额:
$2.25万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2009
资助国家:
日本
项目状态:
已结题
起止时间:
2009 至 2011

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中文摘要
翻译
我们利用ASC缺陷型(ASC-/-)和野生型(ASC+/+)小鼠研究了含有caspase募集结构域(ASC)的凋亡相关斑点样蛋白在小鼠胶原诱导关节炎(CIA)和胶原抗体诱导关节炎(CAIA)进展中的作用。组织免疫组化、血清ELISA分析。我们观察到ASC和IL-1β的表达增加。和IL-18,这表明ASC参与了疾病的发展。接下来,我们证明了与ASC-/-小鼠相比,ASC+/+小鼠的炎症细胞浸润和CIA膝关节软骨/骨破坏明显增加。在ASC+/+和ASC-/- caia小鼠中没有发现这种差异。在膝关节细胞因子表达方面,IL-1β。和IL-18在asc缺失的CIA小鼠中与野生型小鼠相比表达较低,但在两组小鼠的CAIA关节中表达相似。综上所述,我们可以得出结论,ASC参与了CIA的发展,并在II型胶原免疫反应的启动阶段发挥作用。
英文摘要
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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会议论文
ASC Deleted Mice Are Resistant to Collagen-Induced Arthritis.
ASC 缺失小鼠对胶原蛋白诱导的关节炎具有抵抗力。
DOI: --
发表时间: 2009
期刊:
影响因子: --
作者: [Yamazaki H, Takeoka M, Ehara T, Itano N, Kato H, Taniguchi S.]
通讯作者: Taniguchi S.
DOI: 10.1007/s00296-011-1825-y
发表时间: 2012-06
期刊: Rheumatology International
影响因子: 4
作者: [H. Yamazaki;M. Takeoka;M. Kitazawa;T. Ehara;N. Itano;H. Kato;S. Taniguchi]
通讯作者: H. Yamazaki;M. Takeoka;M. Kitazawa;T. Ehara;N. Itano;H. Kato;S. Taniguchi
コラーゲン誘発関節炎におけるアポトーシス制御蛋白ASCの役割
凋亡控制蛋白ASC在胶原诱导的关节炎中的作用
DOI: --
发表时间: 2010
期刊:
影响因子: --
作者: [山崎秀, 加藤博之]
通讯作者: 加藤博之
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