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德斯莫索姆超粘附影响在尾细胞中直接抑制德斯莫格林相互作用

Letyfee Steinert¹, Michael Fuchs¹, Anna M Sigmund¹

¹Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, Ludwig Maximilian University of Munich, Munich, Germany.

The Journal of investigative dermatology

|April 27, 2024

概括

皮细胞的超粘合性通过减少直接抑制desmoglein 3相互作用来保护皮虫的自身抗体. 然而,这种保护作用取决于自身抗体.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
生物物理学的生物物理.

背景情况:

角质细胞在分化过程中发展出超粘附性,改变了脱体德林相互作用.
众所周知,这种超粘合状态可以防止pemphigus vulgaris自身抗体诱导的细胞脱落.
这种保护作用背后的确切机制尚不清楚.

研究的目的:

为了研究质细胞超粘附如何影响pemphigus vulgaris自身抗体诱导的直接抑制desmoglein 3 (DSG3) 相互作用.
为了阐明抗体表位向在超粘附的背景下的作用.

主要方法:

原子力显微镜被用来测量DSG3相互作用的直接抑制.
在非超粘性和超粘性状态下分析了角质细胞.
使用了不同的致病性pemphigus vulgaris自身抗体,针对不同的DSG3域.

主要成果:

超粘附消除了自抗体诱导的细胞间粘附损失和大多数测试的抗体的形态变化.
针对膜近端DSG3域的抗体只在非超粘性细胞中诱导抑制.
一个针对DSG3的N端细胞外域1的抗体 (AK23) 在两个粘附状态中都引起了抑制.
抗体结合性亲和力与desmosomal cadherins并未因附着状态或抗体类型而改变.

结论:

角质细胞的超粘附性降低了受某些pemphigus vulgaris自身抗体直接抑制的易感性,这取决于向的细胞外域.
除了直接抑制之外的其他机制也参与了desmosomal超粘附对pemphigus vulgaris病原体的整体保护作用.

关键词:

德斯莫格莱恩在 3 一个名为Desmosome的.超粘合性超粘合性超粘合性氨酸细胞 (keratinocyte) 是一种细胞.庞菲古斯 (Pemphigus vulgaris) 是一种常见的植物.

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