Naked DNA in cells:An inducer of major histocompatibility complex molecules to evoke autoimmune responses?

作     者：Yuqian Luo Aya Yoshihara Kenzaburo Oda Yuko Ishido Naoki Hiroi Koichi Suzuki 

作者机构：Department of Clinical Laboratory ScienceFaculty of Medical TechnologyTeikyo University Department of Education Planning and DevelopmentFaculty of MedicineToho University Division of DiabetesMetabolism and EndocrinologyDepartment of Internal MedicineToho University 

出 版 物：《World Journal of Translational Medicine》 (世界转化医学杂志)

年 卷 期：2016年第5卷第1期

页      面：46-52页

学科分类：10[医学] 

基　　金：Scientific Research from the Japan Society for the Promotion of Science to Suzuki K No.15K09444 

主　　题：Cytosolic double-stranded DNA Major histocompatibility complex molecules Autoimmune response Antigen presentation Tissue injury 

摘      要：The major histocompatibility complex(MHC) is the exclusive chaperone that presents intracellular antigens,either self or foreign to T ***,aberrant expression of MHC molecules has been reported in various autoimmune target tissues such as thyroid follicular cells in Grave s ***,we review the discovery of an unexpected effect of cytosolic doublestranded DNA(ds DNA),despite its origins,to induce antigen processing and presenting genes,including MHC molecules,in non-immune ***,we highlight several recent studies that suggest cell injury endows thyroid epithelial cells with a phenotype of mature antigen presenting cells by inducing multiple antigen processing and presenting genes via releasing genomic DNA fragments into the *** discuss the possibility that such cytosolic ds DNA,in naked form without binding to histone proteins,might be involved in the development of cell damage-triggered autoimmune *** also discuss the possible molecular mechanism by which cytosolic ds DNA can induce MHC *** is reasonable to speculate that cytosolic ds DNA-induced MHC class Ⅰ is partially due to an autocrine/paracrine effect of type Ⅰ interferon(IFN).While the mechanism of cytosolic ds DNA-induced MHC class Ⅱ expression appears,at least partially,distinct from that mediated by IFN-γ.Further in-depth are required to clarify this picture.