Michelet Xavier, Garg Salil, Wolf Benjamin J, Tuli Amit, Ricciardi-Castagnoli Paola, Brenner Michael B
Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115;
Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115; Division of Cell Biology and Immunology, Institute of Microbial Technology, Chandigarh 160036, India; and.
J Immunol. 2015 Mar 1;194(5):2079-88. doi: 10.4049/jimmunol.1401072. Epub 2015 Jan 30.
Dendritic cells (DCs) are specialized APCs with the ability to prime naive T cells. DCs first sample Ags from the environment and then orchestrate their processing and loading onto MHC class II (MHC II) Ag-presenting molecules in lysosomes. Once MHC II molecules have bound a peptide, the MHC II-peptide complex is delivered to the cell surface for presentation to CD4(+) T cells. Regulation of Ag uptake via macropinocytosis and phagocytosis has been extensively studied, as well as trafficking in early endocytic vesicles notably regulated by the small GTPase Rab5 and its effectors. However, little is known about the regulators of Ag delivery from early endosomes to lysosomal compartments where the proper pH, proteases, MHC II, invariant chain, and HLA-DM reside, awaiting exogenous Ags for loading. In this article, we report the crucial role of the small GTPase ADP-ribosylation factor-like 8b (Arl8b) in MHC II presentation in DCs. We show for the first time, to our knowledge, that Arl8b localizes to MHC II compartments in DCs and regulates formation of MHC II-peptide complexes. Arl8b-silenced DCs display a defect in MHC II-Ag complex formation and its delivery to the cell surface during infection resulting in a defect in T cell recognition. Our results highlight the role of Arl8b as a trafficking regulator of the late stage of complex formation and MHC II presentation in DCs.
树突状细胞(DCs)是具有启动初始T细胞能力的专职抗原呈递细胞(APCs)。DCs首先从环境中摄取抗原,然后精心安排其处理过程,并将其加载到溶酶体中的MHC II类(MHC II)抗原呈递分子上。一旦MHC II分子结合了肽段,MHC II-肽复合物就会被转运到细胞表面,以呈递给CD4(+) T细胞。通过巨胞饮作用和吞噬作用进行的抗原摄取调控已得到广泛研究,早期内吞小泡中的运输也受到显著调控,特别是由小GTP酶Rab5及其效应器调控。然而,对于抗原从早期内体向溶酶体区室的转运调节因子知之甚少,溶酶体区室中存在合适的pH值、蛋白酶、MHC II、恒定链和HLA-DM,等待外源性抗原进行加载。在本文中,我们报道了小GTP酶ADP-核糖基化因子样8b(Arl8b)在DCs的MHC II呈递中的关键作用。据我们所知,我们首次表明Arl8b定位于DCs中的MHC II区室,并调节MHC II-肽复合物的形成。在感染期间,Arl8b沉默的DCs在MHC II-抗原复合物形成及其向细胞表面的转运方面存在缺陷,导致T细胞识别缺陷。我们的结果突出了Arl8b作为DCs中复合物形成后期和MHC II呈递的运输调节因子的作用。