Department of Biological Regulation, The Weizmann Institute of Science, Rehovot 76100, Israel.
Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.
J Immunol. 2020 Nov 15;205(10):2583-2594. doi: 10.4049/jimmunol.1901535. Epub 2020 Oct 16.
Protective MHC class I-dependent immune responses require an overlap between repertoires of proteins directly presented on target cells and cross-presented by professional APC, specifically dendritic cells. How stable proteins that rely on defective ribosomal proteins for direct presentation are captured for cell-to-cell transfer remains enigmatic. In this study, we address this issue using a combination of in vitro (C57BL/6-derived mouse cell lines) and in vivo (C57BL/6 mouse strains) approaches involving stable and unstable versions of OVA model Ags displaying defective ribosomal protein-dependent and -independent Ag presentation, respectively. Apoptosis, but not necrosis, of donor cells was found associated with robust global protein aggregate formation and captured stable proteins permissive for cross-presentation. Potency of aggregates to serve as Ag source was directly demonstrated using polyglutamine-equipped model substrates. Collectively, our data implicate global protein aggregation in apoptotic cells as a mechanism that ensures the overlap between MHC class I epitopes presented directly or cross-presented by APC and demonstrate the unusual ability of dendritic cells to process stable protein aggregates.
保护性 MHC I 类依赖性免疫应答需要靶细胞上直接呈递的蛋白和由专业 APC(特别是树突状细胞)交叉呈递的蛋白之间存在重叠。对于依赖核糖体蛋白缺陷直接呈递的稳定蛋白如何被捕获进行细胞间转移仍然是个谜。在这项研究中,我们使用体外(来自 C57BL/6 的小鼠细胞系)和体内(C57BL/6 小鼠品系)方法的组合来解决这个问题,涉及稳定和不稳定的 OVA 模型抗原,分别显示核糖体蛋白缺陷依赖性和非依赖性抗原呈递。我们发现供体细胞的凋亡而非坏死与强大的全局蛋白聚集体形成有关,并捕获了允许交叉呈递的稳定蛋白。使用带有多聚谷氨酰胺的模型底物直接证明了聚集体作为抗原源的效力。总的来说,我们的数据表明凋亡细胞中的全局蛋白聚集是一种确保 MHC I 类表位直接呈递或由 APC 交叉呈递之间重叠的机制,并证明了树突状细胞处理稳定蛋白聚集体的异常能力。