Gene expression profiling of marrow-derived dendritic cells from non-obese diabetic mice
非肥胖糖尿病小鼠骨髓源性树突状细胞的基因表达谱
基本信息
- 批准号:14570401
- 负责人:
- 金额:$ 1.92万
- 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:2002
- 资助国家:日本
- 起止时间:2002 至 2003
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
In type I diabetes mellitus, dendritic cells play pivotal roles ; they retain capacity to activate autoreactive T cells in the periphery, but are unable to process and/ or resent autoantigens in a tolerogenic fashion. Abnormal phenotype and function of DC from NOD mice have been reported. To characterize molecular changes in Cd11c^+ bone marrow-derived DC from NOD mice, we recently compared the transcript profiles of these cells with those from NON mice. DC from NOD showed 8-fold reduced interleukin 6 (IL-6) mRNA expression compared to those from NON mice. In this study, we examined IL-6 production by DC from NOD mice to confirm the decreased production of this cytokine at protein level. Effect by IL-6 supplementation during differentiation on the phenotype and function of DC was also investigated.Bone marrow cells from 4-week-old female mice were cultivated in the presence of GM-CSF and IL-4 over 6 days, with or without IL-6 supplementation. CD11c^+ DC were sorted by magnetic beads-conjugated with anti-CD11c antibodies (MACS^<TM>).DC from NOD produced significantly lower amount of IL-6 in response to 5 mg/ ml LPS (10970±1685.0 pg/ml) than those from NON (45845±3506.6 pg/ml, p<0.05, Mann-Whitney U test). DC from NOD generated with additional IL-6 (2ng/ml) elicited significantly higher response by CD4^+ cells in the syngeneic mixed lymphocyte reaction (SMLR), measured by succinate-tetrazolium reductase activity (WST-1^<TM>), than those without IL-6 (optic density 0.36±0.031 vs 0.23±0.027, stimulator : responder ratio=1:20,p< 0.05). The up-regulated SMLR was associated with increased median fluorescent intensity of CD80 and CD86 expression by DC (CD80, 116±4.39 vs 92.1±2.75, p<0.05; CD86, 13.2±1.50 vs 9.77±0.289,p<0.05), and significantly lower IFNg production in the SMLR (412.1±40.94 vs 1639±131.6pg/ml,p<0.05).Reduced autocrine secretion of IL-6 by DC may lead to defective phenotype and function of DC, and then to Th1-deviated immune reaction in NOD mice.
在I型糖尿病中,树突状细胞发挥关键作用;它们保留激活外周中自身反应性T细胞的能力,但不能以致耐受性方式处理和/或抵抗自身抗原。据报道,NOD小鼠DC的表型和功能异常。为了表征NOD小鼠骨髓来源的Cd 11 c ^+ DC的分子变化,我们最近比较了NOD小鼠和NON小鼠骨髓来源的DC的转录谱。与来自NON小鼠的DC相比,来自NOD的DC显示白细胞介素6(IL-6)mRNA表达降低8倍。在这项研究中,我们检查了IL-6的生产由DC从NOD小鼠,以确认这种细胞因子的生产在蛋白质水平上的减少。将来自4周龄雌性小鼠的骨髓细胞在存在GM-CSF和IL-4的情况下培养6天,添加或不添加IL-6,观察在分化过程中添加IL-6对DC表型和功能的影响。CD 11 c ^+ DC经磁珠结合抗CD 11 c抗体(MACS^)分选<TM>后,NOD来源的DC对5 mg/ ml LPS产生的IL-6(10970±1685.0 pg/ml)显著低于NON来源的DC(45845±3506.6 pg/ml,p<0.05,Mann-Whitney U检验)。在同系混合淋巴细胞反应(SMLR)中,通过琥珀酸四唑还原酶活性(WST-1^)测定,额外IL-6(2ng/ml)诱导的NOD DC对CD 4 ^+细胞的反应显著<TM>高于不加IL-6的DC(光密度0.36±0.031 vs 0.23±0.027,刺激物:反应物比值=1:20,p< 0.05)。SMLR的上调与DC表达的CD 80和CD 86的中位荧光强度增加有关。(CD80,116±4.39 vs 92.1±2.75,p<0.05; CD 86,13.2±1.50 vs 9.77± 0.289,p <0.05),并且在SMLR中显著降低IFNg产生(412.1±40.94 vs 1639±131.6pg/ml,p<0.05)。NOD小鼠DC自分泌IL-6减少可能导致DC表型和功能缺陷,进而导致免疫反应向Th 1方向偏移。
项目成果
期刊论文数量(12)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Takahashi K, Satoh J et al.: "Promoter polymorphism of SLC11A1 (formerly NRAMP1) confers susceptibility to autoimmune type 1 diabetes mellitus in Japanese"Tissue Antigens. 63(3). 231-236 (2004)
Takahashi K、Satoh J 等人:“SLC11A1(以前称为 NRAMP1)的启动子多态性赋予日本人对自身免疫性 1 型糖尿病的易感性”组织抗原。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
高橋和眞: "Natural resistance associates macrophage protein 1(NRAMP1)遺伝子プロモーターの新しい多型と日本人1型糖尿病との関連"Journal of the Japan Diabetes Society. 45・2. S-93 (2002)
Kazuma Takahashi:“巨噬细胞蛋白 1 (NRAMP1) 基因启动子的自然抵抗力的新多态性及其与日本人 1 型糖尿病的关系”,日本糖尿病学会杂志 45・2(2002 年)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
高橋和眞: "1型糖尿病の予知と予防"Diabetes Frontier. 14. 17-28 (2003)
Kazumasa Takahashi:“1 型糖尿病的预测和预防”糖尿病前沿 14. 17-28 (2003)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Takahashi K, Satoh J et al.: "Promoter polymorphism of SLC11A1 (formerly NRAMP1) confers susceptibility to autoimmune type 1 diabetes mellitus_in Japanese."Tissue Antigens. 63・3. 231-236 (2004)
Takahashi K、Satoh J 等人:“SLC11A1(以前称为 NRAMP1)的启动子多态性赋予自身免疫性 1 型糖尿病的易感性_日语。”组织抗原 63・3(2004)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
K.Takahashi: "Redused diabetogenic effector cells in the nod mice lacking interferon regulatory factor-1"Diabetes Metabolism Research and Reviews. 18・4. S56 (2002)
K. Takahashi:“缺乏干扰素调节因子-1 的 nod 小鼠中的糖尿病效应细胞的减少”糖尿病代谢研究与评论 S56 (2002)。
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- 影响因子:0
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TAKAHASHI Kazuma其他文献
続「〇歳からの草木染」藍を育て,スクモを作り,藍染をするこどもたち(その3)
续“适合 0 岁及以上的植物染色” 儿童种植靛蓝、制作蓝靛和染色靛蓝(第 3 部分)
- DOI:
- 发表时间:
2022 - 期刊:
- 影响因子:0
- 作者:
TAKAHASHI Kazuma;HATTORI Tatsumi;DOMAN Keisuke;KAWANISHI Yasutomo;HIRAYAMA Takatsugu;IDE Ichiro;DEGUCHI Daisuke;MURASE Hiroshi;佐々木和也(監修) - 通讯作者:
佐々木和也(監修)
Multi-lapped directional wavelet transforms and their applications to image analysis
多层定向小波变换及其在图像分析中的应用
- DOI:
- 发表时间:
2017 - 期刊:
- 影响因子:0
- 作者:
TAKAHASHI Kazuma;HATTORI Tatsumi;DOMAN Keisuke;KAWANISHI Yasutomo;HIRAYAMA Takatsugu;IDE Ichiro;DEGUCHI Daisuke;MURASE Hiroshi;Kensuke Fujinoki - 通讯作者:
Kensuke Fujinoki
TAKAHASHI Kazuma的其他文献
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{{ truncateString('TAKAHASHI Kazuma', 18)}}的其他基金
A unique CD204^+ subpopulation of dendritic cells in NOD mice
NOD 小鼠中独特的 CD204^ 树突状细胞亚群
- 批准号:
17590911 - 财政年份:2005
- 资助金额:
$ 1.92万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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- 批准号:31272541
- 批准年份:2012
- 资助金额:82.0 万元
- 项目类别:面上项目
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