Development of autoimmune mouse model by viral factors

本研究阐明细小病毒非结构（NS）蛋白诱导T淋巴细胞DNA甲基化，引起细胞凋亡抵抗和细胞增殖的变化。此外，在体内检查了 NS 对胶原诱导的关节炎发生率的可能影响。感染NS-EGFP表达载体的小鼠T淋巴细胞大部分引起凋亡，存活的细胞通过DNA甲基化抑制Bmper表达。这些细胞获得了对细小病毒再次感染的抵抗力。感染NS-EGFP表达载体的DBA/1小鼠出现胶原诱导的关节炎，但其发生率与对照小鼠无显着差异。

In the present study, it was elucidated that parvoviral nonstructure (NS) protein induced DNA methylation in T lymphocytes and caused change of apoptosis resistancy and cell proliferation. Moreover, a possible effect of NS for incidence of collagen-induced arthritis was examined in vivo. The most of mouse T lymphocytes infected with NS-EGFP expression vector caused apoptosis, and the survived cells suppressed Bmper expression by DNA methylation. These cells acquired to be resistant for parvoviral re-infection. DBA/1 mice infected with NS-EGFP expression vector developed collagen-induced arthritis, though there was no significant difference on incidence of them to that of the control.