Detection of periodontal disease activity by T cell receptor repertoire and cytokine profile of infiltrating T cells

通过 T 细胞受体库和浸润 T 细胞的细胞因子谱检测牙周病活动

基本信息

  • 批准号:
    05671593
  • 负责人:
  • 金额:
    $ 1.41万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
  • 财政年份:
    1993
  • 资助国家:
    日本
  • 起止时间:
    1993 至 1994
  • 项目状态:
    已结题

项目摘要

In order to characterize the T cells infiltrating gingival tissues with periodontitis, T cell receptor repertoire and cytokine profile were investigated by means of immunohistological procedure. Periodontitis tissues were obtained at the time of periodontal surgery after completion of initial therapy. Gingivitis tissues as a control were also obtained from non-periodontitis lesions. Serial cryostat sections from each specimen were immunostained for TCR V gene products (Valpha2, Vbeta5.2-3, Vbeta5.3, Vbeta5.1, Vbeta6.7, Vbeta8, Vbeta12) and cytokines (IL-2, IFN-gamma, IL-4, IL-6) with alkaline phosphataseanti alkaline phosphatase method. Relative percentages were caluclated by dividing the number of each positive cell by total number of CD3 positive cells. Moreover, for comparison between gingival tissues and circulating pool, peripheral blood mononuclear cells from both groups were analyzed for the TCR repertoire by flow cytometry. The pattern of each TCR V gene product expression in i … More nflamed gingiva exhibited individual variation, nevertheless a consistent pattern emerged. The Vbeta5 subfamily and Vbeta6.7 were frequently used repertoires in gingiva, whereas the Valpha2 and Vbeta8 subfamily were underexpressed in most cases. Furthermore, the TCR V gene product expression in gingival tissue was biased compared with autologous peripheral blood. Three out of 10 periodontitis subjects showed 1 or 2 strikingly overrepresented repertoire comparatively with autologous blood. In these 3 subjects Vbeta6.7 was overexpressed in two cases and Vbeta5.2-3, Vbeta8 and Vbeta12 were overexpressed in one case. With respect to the cytokine profile, the proportion of IL-4- and IL-6- producing T cells was higher in periodontitis than in gingivitis. Moreover, a siginificant positive correlation between the proportion of IL-4-producing cells and the B cell : T cell ratio was noted. These data suggest that gingival T cells are not randomly mobilized from peripheral blood and that local events influence the TCR repertoire at the level of T cell recruitment or T cell expansion and the functional subsets of those T cells are Th2 type. Less
为了表征牙周炎浸润牙龈组织的T细胞,通过免疫组织学程序研究了T细胞受体库和细胞因子谱。初始治疗完成后,在牙周手术时获得牙周炎组织。牙龈炎组织还从非周期性炎病变中获得。对TCR V基因产物(valpha2,vbeta5.2-3,vbeta5.3,vbeta5.1,vbeta5.1,vbeta6.7,vbeta8,vbeta8,vbeta12)和细胞因子(IL-2,ifn-2,ifn-gamma,ifn-gamma groundi flochiation)(IL-2,IL-4-6),对每个样品的串行低温抑制切片进行免疫染色(valpha2,vbeta5.2-3,vbeta5.2-3,vbeta5.3,vbeta5.3,vbeta5.3,vbeta5.1,vbeta6.7,vbeta12) 方法。通过将每个正细胞的数量除以CD3阳性细胞的总数,从而将相对百分比归类。此外,为了比较牙龈组织和循环池,通过流式细胞仪分析了两组的外周血单核细胞的TCR库。 I…中每个TCR V基因产物表达的模式暴露了个体变异,但出现了一致的模式。 VBETA5亚家族和VBETA6.7经常在gingiva中使用,而在大多数情况下,valpha2和valpha2和vbeta8亚家族都不被渗透。此外,与自体外周血相比,牙龈中的TCR V基因产物产物表达有偏见。在10个牙周炎受试者中,有3名与自体血相比表现出1或2个惊人的过分代表性曲目。在这三个受试者中,VBETA6.7在两种情况下过表达,VBETA5.2-3,VBETA8和VBETA12在一个情况下过表达。关于细胞因子的特征,牙周炎的IL-4-和IL-6-产生T细胞的比例高于牙龈炎。此外,注意到IL-4产生细胞的比例与B细胞:T细胞比率之间存在毫无用处的阳性相关性。这些数据表明,牙龈T细胞不是从外围血液中随机动员的,并且局部事件在T细胞募集或T细胞膨胀水平上影响TCR库,这些T细胞的功能子集是Th2类型的。较少的

项目成果

期刊论文数量(16)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Kazuhisa Yamazaki: "IL-4 and IL-6-producing cells in human periodontal disease tissue" Journal of Oral Pathology and Medicine. 23. 347-353 (1994)
Kazuhisa Yamazaki:“人类牙周病组织中产生 IL-4 和 IL-6 的细胞”《口腔病理学与医学杂志》。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Nakajima, T., Yamazaki, K., Hara, K: "Biase T cell receptor V gene usage in tissues with periodontal disease" J.Periodont.Res. (in press.). (1995)
Nakajima, T.、Yamazaki, K.、Hara, K:“偏向 T 细胞受体 V 基因在牙周病组织中的使用”J.Periodont.Res。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Toshihiko Aoyagi: "IL-4 and IL-6-producing memory T-cells in peripheral blood and gingival tissues in periodontitis patients with hight serum antibody titers to Perphyromonas gingivalis." Oral Microbiology and Immunology. (印刷中).
Toshihiko Aoyagi:“牙周炎患者的外周血和牙龈组织中产生 IL-4 和 IL-6 的记忆 T 细胞,具有高血清牙龈卟啉单胞菌抗体滴度。”
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Takako Nakajima: "Biased T cell receptor Vgene usage in tissues with periodontal disease" Journal of Periodontal Research. (印刷中).
Takako Nakajima:“牙周病组织中偏向 T 细胞受体 V 基因的使用”《牙周研究杂志》(正在出版)。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Kazuhisa Yamazaki: "Immunohistological analysis of T-cell functional subsets in chronic inflammatory periodontal disease." Clinical and Experimental Immunology. 99. 384 (1995)
Kazuhisa Yamazaki:“慢性炎症性牙周病 T 细胞功能亚群的免疫组织学分析。”
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  • 影响因子:
    0
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YAMAZAKI Kazuhisa其他文献

YAMAZAKI Kazuhisa的其他文献

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{{ truncateString('YAMAZAKI Kazuhisa', 18)}}的其他基金

New hypothesis for the pathogenesis of periodontal medicine
牙周医学发病机制的新假说
  • 批准号:
    25670882
  • 财政年份:
    2013
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Analysis of the pathway from periodontal disease to lipid metabolism perturbation
牙周病与脂质代谢紊乱的通路分析
  • 批准号:
    23390476
  • 财政年份:
    2011
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Establishment of the new concept "pathogenic mechanism of periodontal disease by the induction of senescence of the tissues".
建立“诱导组织衰老导致牙周病发病机制”新概念。
  • 批准号:
    23659974
  • 财政年份:
    2011
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Clarification of the pathogenicity of periodontal disease involving exacerbation of metabolic syndrome ; an approach based on immunological characteristics.
阐明涉及代谢综合征恶化的牙周病的致病性;
  • 批准号:
    19390536
  • 财政年份:
    2007
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Clarification of the mechanisms for connective tissue destruction and alveolar bone resorption in periodontal disease by comprehensive analysis of infiltrating T cells using immunological and molecular biological techniques
利用免疫学和分子生物学技术对浸润性 T 细胞进行综合分析,阐明牙周病中结缔组织破坏和牙槽骨吸收的机制
  • 批准号:
    16390613
  • 财政年份:
    2004
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Molecular biological and immunological analysis for the relationship between periodontal disease and atherosclerosis
牙周病与动脉粥样硬化关系的分子生物学和免疫学分析
  • 批准号:
    13470462
  • 财政年份:
    2001
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Analysis of antigen receptor genes of T cells specific for the periodontal disease
牙周病特异性T细胞抗原受体基因分析
  • 批准号:
    10470458
  • 财政年份:
    1998
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).
Characteristic T cell receptor repertoire and cytokine profile of infiltrating T cells in chronic inflammatory periodontal disease
慢性炎症性牙周病浸润性 T 细胞的特征性 T 细胞受体库和细胞因子谱
  • 批准号:
    07457454
  • 财政年份:
    1995
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Establishment of Diagnostic Methods of Periodontal Disease Basing on the Alteration of Immunocompetent Cells
基于免疫活性细胞变化的牙周病诊断方法的建立
  • 批准号:
    03807127
  • 财政年份:
    1991
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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人类急性牙龈炎系统生物学
  • 批准号:
    484000
  • 财政年份:
    2023
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    $ 1.41万
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人群牙龈炎症反应速率和水平差异的机制
  • 批准号:
    10596337
  • 财政年份:
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Determination of structure-function relationships and role in virulence of a MerR-type regulator that mediates zinc tolerance in Streptococcus mutans
确定介导变形链球菌锌耐受性的 MerR 型调节因子的结构-功能关系及其毒力作用
  • 批准号:
    10749982
  • 财政年份:
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