CAJ | 학술논문

目的探讨在狼疮小鼠脾细胞中是否存在 IL-12通过 Lck/p38/c-jun传递信号及其对脾细胞的影响。方法以慢性移植物抗宿主病 (graft versus host disease, GVHD)小鼠为狼疮小鼠模型，分别采用放射自显影、 Western blot和 Northern blot，检测培养的脾细胞中 Lck的活性、 p38磷酸化活化及 c-jun基因表达的变化。结果狼疮小鼠脾细胞经 IL-12刺激后，与正常对照组相比较， Lck的活性增高、 p38异常活化， c-jun mRNA的水平增高。加入 Lck抑制剂 PP1组 Lck的活性及 p38磷酸化消失，无 c-jun基因的表达；加入 p38抑制剂 SB203580组亦无 p38磷酸化及 c-jun基因的表达。结论狼疮小鼠的脾细胞异常， IL-12可通过 Lck/ p38/c-jun在细胞内传递信号，直接参与免疫损伤。
목적탐토재랑창소서비세포중시부존재 IL-12통과 Lck/p38/c-jun전체신호급기대비세포적영향。방법이만성이식물항숙주병 (graft versus host disease, GVHD)소서위랑창소서모형，분별채용방사자현영、 Western blot화 Northern blot，검측배양적비세포중 Lck적활성、 p38린산화활화급 c-jun기인표체적변화。결과랑창소서비세포경 IL-12자격후，여정상대조조상비교， Lck적활성증고、 p38이상활화， c-jun mRNA적수평증고。가입 Lck억제제 PP1조 Lck적활성급 p38린산화소실，무 c-jun기인적표체；가입 p38억제제 SB203580조역무 p38린산화급 c-jun기인적표체。결론랑창소서적비세포이상， IL-12가통과 Lck/ p38/c-jun재세포내전체신호，직접삼여면역손상。
Aim To investigate whether there is IL-12 signaling pathway through lck/P38/c-jun in splenic cells obtained from lupus mouse and its effect on splenic cells. Methods Mice with graft versus host disease were used as lupus nephritis model. Activity of Lck tyrosine kinase, p38 phosphorylation and mRNA expression of c-jun in splenic cells were determined by autoradiography, Western blot and Northern blot, respectively. Results There were higher levels of Lck activity, p38 phosphorylation and c-jun expression of IL-12-stimulated splenic cells from lupus model when compared with that observed in similarly treated splenic cells from normal control. The Lck activity and p38 phosphorylation were almost inhibited by Lck inhibitor PP1, on the other hand, p35 specific inhibitor SB203580 decreased phosphorylation of p38. In addition, expression of c-Jun was also inhibited by PP1 or SB203580 although splenic cells were stimulated with IL-12. Conclusion Aberrant murine splenic cell, IL-12-me-diated intracelluar signaling pathway through lck/p38/c-Jun were involved in immunologic damage.