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Arthritis Rheumatol:组织驻留记忆CD8+T细胞介导干燥综合征小鼠模型中的唾液腺损伤

2018-07-24 xiangting MedSci原创

这项研究数据揭示了SS中CD8+T细胞在唾液腺病理中的致病意义。针对CD8+T细胞的治疗可能是人类SS的合理疗法。

尽管CD4+T细胞在干燥综合征(SS)病理学中的作用已被证实,但CD8+T细胞的致病意义尚不清楚。这项研究目的是探讨CD8+T细胞在SS进展中的作用。

使用流式细胞术和免疫荧光检测原发性SS患者唇腺内的T细胞浸润。同时,使用p40-/-CD25-/-小鼠作为SS鼠科模型。此外,分别将CD4、CD8a和IFN-γKO小鼠与p40-/-CD25-/-小鼠进行杂交,以研究特定谱系亚群的致病意义,其中包括功能性唾液、组织病理学和血清学数据。使用CD8+T细胞特异性耗竭抗体评估这种潜在的治疗策略。

SS患者唇腺中的组织驻留记忆表型的CD8+T细胞远远超过CD4+T细胞,并主要共存于唾液导管上皮细胞和腺泡细胞。此外,IFN-γ生成显著升高的驻留表型CD69+CD103+/-浸润CD8+T细胞在SS小鼠模型的下颌下腺中占主导。敲除CD8a抑制了这些小鼠中SS的进展。敲除IFN-γ降低了CD8+T细胞浸润和腺体破坏。更重要的是,即使在疾病起病后,耗竭CD8+T细胞也可以完全保护小鼠免于SS。 

这项研究数据揭示了SS中CD8+T细胞在唾液腺病理中的致病意义。针对CD8+T细胞的治疗可能是人类SS的合理疗法。

原始出处:

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    2019-01-19 gds2009
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  4. 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    2018-07-26 zhaojie88
  5. 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  6. 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  7. 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topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=null, createdBy=f0620, createdName=CHANGE, createdTime=Tue Jul 24 13:35:00 CST 2018, time=2018-07-24, status=1, ipAttribution=)]
    2018-07-24 CHANGE

    梅斯里提供了很多疾病的模型计算公式,赞一个!

    0

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