Pathological analysis of skin fibrosis, focused on type 2 innate immune lymphoid cells
皮肤纤维化病理分析,重点关注2型先天免疫淋巴细胞
基本信息
- 批准号:24659520
- 负责人:
- 金额:$ 2.41万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Challenging Exploratory Research
- 财政年份:2010
- 资助国家:日本
- 起止时间:2010 至 2012
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
We have studied the mechanism of cryopyrin-associated periodicsyndrome (CAPS), in which an active mutant of NLRP3 spontaneously forms inflammasome andinduces hyper-production of IL-1β. This study led us to focus on the pivotal role of IL-1 in skindiseases. Recently, people pay attention to another IL-1 family molecule, IL-33, because IL-33released from damaged cells in inflammation is critically involved in inflammatory response by aproduction of Th2 cytokines and a degranulation of mast cells. In addition, IL-33 induces a largeamount of Th2 cytokine production from innate lymphoid cells (ILCs). ILCs are newly identifiedlymphoid lineage cells, keep haematopoietic stem cell markers and are present in the mesentericfat-associated lymphoid clusters.Interestingly, the structure of mesenteric fat-associated lymphoid clusters shares thesimilar feature with that of aggregated clusters of lymphoid cells in subcutaneous fat in localizedscleroderma. Also serum IL-33 is reported to be elevated in scleroderma and serum levels of IL-33is well correlated with the severity of cutaneous sclerosis in scleroderma. Therefore, we studied therole of IL-33 in bleomycin-induced scleroderma murine model by comparing the effect in IL-33deficient mice and wild type mice.Six weeks after bleomycin-treatment, we obtained localized cutaneous sclerosisaccompanied with increased skin fibrosis in wild type mice. However, lymphoid cell infiltrationwas not observed in the skin lesion. Unfortunately, the cutaneous sclerosis including histologicalfeatures in IL-33 deficient mice was almost identical to that in wild type mice. We concluded from these results that we should verify the cutaneous role of IL-33 by focusing on Th2 immuneresponse, and now we are establishing such a model to confirm it.
我们研究了cryopyrin-associated acute myocardial infarction syndrome(CAPS)的发病机制,其中NLRP 3的活性突变体自发形成炎性小体并诱导IL-1β的过度产生。这项研究使我们关注IL-1在皮肤病中的关键作用。近年来,IL-1家族的另一分子IL-33引起了人们的关注,因为IL-33在炎症中通过产生Th 2细胞因子和肥大细胞脱颗粒而参与炎症反应。此外,IL-33还能诱导先天性淋巴样细胞(ILC)产生大量Th 2细胞因子。ILC是新近发现的淋巴系细胞,具有造血干细胞标记,存在于肠系膜脂肪相关淋巴细胞簇中,有趣的是,肠系膜脂肪相关淋巴细胞簇的结构与局限性硬皮病皮下脂肪淋巴细胞簇的结构相似。此外,据报道,硬皮病患者血清IL-33水平升高,且血清IL-33水平与硬皮病患者皮肤硬化的严重程度密切相关。因此,我们研究了IL-33在博莱霉素诱导的硬皮病小鼠模型中的作用,通过比较IL-33缺陷小鼠和野生型小鼠的作用,在博莱霉素治疗后6周,我们在野生型小鼠中获得了局部皮肤硬化伴皮肤纤维化增加。皮损中未见淋巴样细胞浸润。不幸的是,IL-33缺陷小鼠的皮肤硬化包括组织学特征与野生型小鼠几乎相同。从这些结果我们得出结论,我们应该通过关注Th 2免疫反应来验证IL-33的皮肤作用,现在我们正在建立这样的模型来证实它。
项目成果
期刊论文数量(21)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
IL-33と慢性アレルギー炎症.
IL-33 和慢性过敏性炎症。
- DOI:
- 发表时间:2012
- 期刊:
- 影响因子:0
- 作者:Ohno T;Morita H;Arae K;Matsumoto K;Nakae S.;中野倫代,神戸直智;神戸直智,中村悠美;大野建州,東みゆき,中江進;新江賢,大野建州,森田英明,松本健治,中江進;森田英明,新江賢,大野建州,松本健治,中江進;大野建州,森田英明,新江賢,松本健治,中江進;大野建州,森田英明,新江賢,松本健治,中江進;大野建州,東みゆき,中江進;中野倫代,神戸直智.;神戸直智,中村悠美.;大野建州,東みゆき,中江 進.
- 通讯作者:大野建州,東みゆき,中江 進.
IL-33と慢性アレルギー炎症
IL-33 与慢性过敏性炎症
- DOI:
- 发表时间:2012
- 期刊:
- 影响因子:0
- 作者:Ohno T;Morita H;Arae K;Matsumoto K;Nakae S.;中野倫代,神戸直智;神戸直智,中村悠美;大野建州,東みゆき,中江進
- 通讯作者:大野建州,東みゆき,中江進
IL-33による慢性アレルギー炎症
IL-33引起的慢性过敏性炎症
- DOI:
- 发表时间:2012
- 期刊:
- 影响因子:0
- 作者:Ohno T;Morita H;Arae K;Matsumoto K;Nakae S.;中野倫代,神戸直智;神戸直智,中村悠美;大野建州,東みゆき,中江進;新江賢,大野建州,森田英明,松本健治,中江進;森田英明,新江賢,大野建州,松本健治,中江進;大野建州,森田英明,新江賢,松本健治,中江進;大野建州,森田英明,新江賢,松本健治,中江進
- 通讯作者:大野建州,森田英明,新江賢,松本健治,中江進
IL-33によるマスト細胞・好塩基球の活性化とアレルギー疾患.
IL-33 激活肥大细胞和嗜碱性粒细胞和过敏性疾病。
- DOI:
- 发表时间:2012
- 期刊:
- 影响因子:0
- 作者:Ohno T;Morita H;Arae K;Matsumoto K;Nakae S.;中野倫代,神戸直智;神戸直智,中村悠美;大野建州,東みゆき,中江進;新江賢,大野建州,森田英明,松本健治,中江進;森田英明,新江賢,大野建州,松本健治,中江進;大野建州,森田英明,新江賢,松本健治,中江進;大野建州,森田英明,新江賢,松本健治,中江進;大野建州,東みゆき,中江進;中野倫代,神戸直智.;神戸直智,中村悠美.;大野建州,東みゆき,中江 進.;新江 賢,大野建州,森田英明,松本健治,中江 進.;森田英明,新江賢,大野建州,松本健治,中江 進.
- 通讯作者:森田英明,新江賢,大野建州,松本健治,中江 進.
IL-33とアレルギー
IL-33 和过敏
- DOI:
- 发表时间:2011
- 期刊:
- 影响因子:0
- 作者:Takei T;Morozumi M;Kadota K;Miyamae T;Yokota S;Ubukata K;Iwata S;Takahashi T;善本知広
- 通讯作者:善本知広
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KAMBE Naotomo的其他文献
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{{ truncateString('KAMBE Naotomo', 18)}}的其他基金
Molecular mechanism on granuloma formation based on the analysis with cellular and molecular biology
基于细胞分子生物学分析的肉芽肿形成的分子机制
- 批准号:
23390280 - 财政年份:2011
- 资助金额:
$ 2.41万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Gene analysis of epidermal gap junction and pathological search for palmoplantar hyperkeratosis associated with hearing impairments
表皮间隙连接基因分析及听力障碍相关掌跖角化过度的病理学研究
- 批准号:
23659542 - 财政年份:2011
- 资助金额:
$ 2.41万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Molecular mechanism of cell death induced by the activation of intracellular pattern recognition receptor, cryopyrin
细胞内模式识别受体cryopyrin激活诱导细胞死亡的分子机制
- 批准号:
19591303 - 财政年份:2007
- 资助金额:
$ 2.41万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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