Nat Commun：整合素可使T细胞不再产生免疫应答

2014-11-04 佚名生物谷

2014年11月3日讯 /生物谷BIOON/ --近日研究发现，当整合素释放它们的配体和树突细胞内的肌动蛋白细胞骨架时，另一个细胞表面受体gm - csf的活性就会增强，增强的信号诱导树突状细胞刺激淋巴结激活T细胞。整合素是一种粘附分子并能够在细胞表面进行表达。它们在细胞“整合”的外部与细胞内部细胞骨架中起着非常重要的作用。beta2-整联蛋白系在树突状细胞中有较高量的表达，这对免疫应答

2014年11月3日讯 /生物谷BIOON/ --近日研究发现，当整合素释放它们的配体和树突细胞内的肌动蛋白细胞骨架时，另一个细胞表面受体gm - csf的活性就会增强，增强的信号诱导树突状细胞刺激淋巴结激活T细胞。

整合素是一种粘附分子并能够在细胞表面进行表达。它们在细胞“整合”的外部与细胞内部细胞骨架中起着非常重要的作用。beta2-整联蛋白系在树突状细胞中有较高量的表达，这对免疫应答非常重要。树突细胞在发炎组织中刺激抗原产生然后转移到淋巴结中，在淋巴结中提呈抗原到T细胞中，之后激活它们用以抵抗感染。

Susanna Fagerholm博士的研究组发现的首要步骤是在激活链中整合素不能再控制组织中的配体和树突细胞内的肌动蛋白细胞骨架。

“这将导致树突细胞中gm - csf表面受体信号增强。信号增强导致重组树突状细胞发育成熟并诱发它们转移到淋巴结并激活T细胞。”Susanna Fagerholm说。

Susanna Fagerholm研究小组用新型敲入技术将beta2整联蛋白敲入到小鼠模型体内，并在其体内做免疫分析，之后结合下一代核糖核酸测序技术用来研究树突细胞中beta2整联蛋白的作用。

“更好的理解这一连串的实验过程有助于在靶向疗法的设计中帮助阻止不必要的免疫反应发生，比如那些与自身免疫有关的反应。这种类型的研究也有助于设计更有效的癌症免疫疗法”。

原始出处

Morrison VL1, James MJ2, Grzes K3, Cook P4, Glass DG5, Savinko T2, Lek HS3, Gawden-Bone C6, Watts C6, Millington OR7, MacDonald AS4, Fagerholm SC1.Loss of beta2-integrin-mediated cytoskeletal linkage reprograms dendritic cells to a mature migratory phenotype.Nat Commun. 2014 Oct 28

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好好学习

117 0
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2016-03-17 忠诚向上

好好学习

80 0
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2016-03-17 忠诚向上

好好学习

118 0
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2016-03-17 忠诚向上

好好学习

86 0
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2016-03-17 忠诚向上

好好学习

62 0
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2016-03-17 忠诚向上

好好学习

67 0
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2016-03-17 忠诚向上

好好学习

64 0

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