摘要
目的 观察胃良、恶性上皮组织表达GrB的情况并探讨其对局部免疫反应的影响。方法 采用免疫组织化学染色S P法检测慢性胃炎 (8例 )及胃癌组织 (35例 )中GrB的表达及组织中浸润的GrB+ CTL、NK细胞密度。结果 (1)胃良、恶性上皮组织均有GrB表达 ,阳性率分别是 6 2 5 % (5 8)和 4 0 % (14 35 ) ,差异无显著意义 (χ2 =0 5 8,P >0 0 5 ) ;(2 )胃癌组GrB+ CTL、NK细胞密度高于良性病变组 ,但差异亦无显著意义 (t=1 6 3,P >0 0 5 ) ;(3)癌组织GrB表达及其浸润的GrB+ CTL、NK细胞密度在各临床病理组间差异均无统计学意义 ,但前者在年龄组的差异接近检验水准 (P =0 0 6 ) ;(4)GrB+ 胃癌与GrB- 比较 ,其间质GrB+ CTL、NK细胞密度显著下降 (t=1 89,P <0 0 5 ) ,两者呈显著负相关 (γs=- 0 5 5 ,P <0 0 0 1)。结论 GrB表达可能是胃上皮细胞恶性转化过程伴随的改变之一 ,为转化细胞提供免疫保护 ,并可能是肿瘤逃逸免疫应答的新的分子机制。
Objective To observe whether benign and malignant gastric epithelial cells express cytotoxic protein GrB and investigate its effect on local immune response Methods Immunohistochemical staining for GrB was performed on paraffin sections from 8 specimens of chronic superficial gastritis (CSG) and 35 specimens of gastric caner (GC) to detect the GrB expression and density of infiltration by GrB +cytotoxic lymphocyte (CTL) and NK Results (1) GrB was expressed in both benign and malignant gastric epithelial cells with the expression rates of 62 5% (5/8) and 40% (14/35) respectively (χ 2=0 58, P >0 05) (2) The density of infiltration by GrB +CTL and NK in GC group was greater than that in CSG group, however without significant difference ( t =1 628, P >0 05) (3) The density of infiltration by GrB +CTL and NK, and GrB expression in GC showed no significant difference among different clinicopathological variables except age The GrB expression rate in age group impended to the marked level of test ( P =0 06) (4) The density of infiltration by GrB +CTL and NK in GrB positive GC group was significantly less than that in GrB negative GC group ( t =1 89, P <0 05) The density of infiltration by GrB +CTL and NK showed a significantly negative correlation with GrB expression in GC (γ s=-0 55, P <0 001) Conclusion GrB expression in gastric epithelial cell may be one of the accompanying changes in the course of malignant transformation of cells and play an important role in inhibiting local immune response, and it can be speculated as a novel molecule mechanism for tumor to escape immune surverllance
出处
《中华医学杂志》
CAS
CSCD
北大核心
2002年第14期966-969,共4页
National Medical Journal of China
