中华口腔医学杂志
中華口腔醫學雜誌
중화구강의학잡지
Chinese Journal of Stomatology
2010年
4期
219-222
,共4页
雷蕾%谭为霞%周序珑%郑佩娥
雷蕾%譚為霞%週序瓏%鄭珮娥
뢰뢰%담위하%주서롱%정패아
扁平苔藓,口腔%Fas配体蛋白质%激活诱导细胞死亡
扁平苔蘚,口腔%Fas配體蛋白質%激活誘導細胞死亡
편평태선,구강%Fas배체단백질%격활유도세포사망
Lichen planus,oral%Fas ligang protein%Activation-induced cell death
目的 检测Fas及Fas配体(Fas ligand,FasL)在口腔扁平苔藓(oral lichen planus,OLP)固有层淋巴细胞中的蛋白表达,探讨Fas、FasL和活化诱导的细胞死亡(activation-induced cell death,AICD)与OLP发病的关系.方法 采用脱氧核糖核苷酸末端转移酶介导的原位缺口末端标记法检测31例OLP和10例正常口腔黏膜(normal oral mucosa,NOM)中淋巴细胞凋亡情况;分别使用免疫组化法检测组织总淋巴细胞及CD8~+、CD4~+T细胞Fas、FasL的表达.结果 OLP与NOM固有层淋巴细胞凋亡率[分别为(1.9±1.8)%、(11.5±9.0)%]差异有统计学意义(P=0.013).OLP淋巴细胞Fas、FasL表达与NOM组相比明显增强[阳性表达率分别为52%(16/31)、71%(22/31),P值分别为0.005、0.000].OLP中CD8~+与Fas~+细胞双阳性表达率为10%,与NOM组相比无明显升高(P=0.313),而CD8~+与FasL~+细胞双阳性表达率[58%(3/31)]显著升高(P=0.002).CD4~+与Fas~+细胞双阳性表达率为35%(11/31),较NOM组显著升高(P=0.031),其中网纹型的表达明显升高(阳性表达为8/19,P=0.019),但糜烂、萎缩型的表达无显著升高(阳性表达为3/12,P=0.097).CD4~+与FasL~+表达率为16%(5/31),与NOM组相比无明显增强(P=0.182).结论 OLP淋巴细胞凋亡低下;OLP中T细胞亚群Fas、FasL表达不均衡,CD8~+细胞和萎缩、糜烂型OLP中CD4~+细胞可能逃逸AICD,与炎症的持续和进展有关;网纹型OLP中部分CD4~+T细胞可能经历AICD.
目的 檢測Fas及Fas配體(Fas ligand,FasL)在口腔扁平苔蘚(oral lichen planus,OLP)固有層淋巴細胞中的蛋白錶達,探討Fas、FasL和活化誘導的細胞死亡(activation-induced cell death,AICD)與OLP髮病的關繫.方法 採用脫氧覈糖覈苷痠末耑轉移酶介導的原位缺口末耑標記法檢測31例OLP和10例正常口腔黏膜(normal oral mucosa,NOM)中淋巴細胞凋亡情況;分彆使用免疫組化法檢測組織總淋巴細胞及CD8~+、CD4~+T細胞Fas、FasL的錶達.結果 OLP與NOM固有層淋巴細胞凋亡率[分彆為(1.9±1.8)%、(11.5±9.0)%]差異有統計學意義(P=0.013).OLP淋巴細胞Fas、FasL錶達與NOM組相比明顯增彊[暘性錶達率分彆為52%(16/31)、71%(22/31),P值分彆為0.005、0.000].OLP中CD8~+與Fas~+細胞雙暘性錶達率為10%,與NOM組相比無明顯升高(P=0.313),而CD8~+與FasL~+細胞雙暘性錶達率[58%(3/31)]顯著升高(P=0.002).CD4~+與Fas~+細胞雙暘性錶達率為35%(11/31),較NOM組顯著升高(P=0.031),其中網紋型的錶達明顯升高(暘性錶達為8/19,P=0.019),但糜爛、萎縮型的錶達無顯著升高(暘性錶達為3/12,P=0.097).CD4~+與FasL~+錶達率為16%(5/31),與NOM組相比無明顯增彊(P=0.182).結論 OLP淋巴細胞凋亡低下;OLP中T細胞亞群Fas、FasL錶達不均衡,CD8~+細胞和萎縮、糜爛型OLP中CD4~+細胞可能逃逸AICD,與炎癥的持續和進展有關;網紋型OLP中部分CD4~+T細胞可能經歷AICD.
목적 검측Fas급Fas배체(Fas ligand,FasL)재구강편평태선(oral lichen planus,OLP)고유층림파세포중적단백표체,탐토Fas、FasL화활화유도적세포사망(activation-induced cell death,AICD)여OLP발병적관계.방법 채용탈양핵당핵감산말단전이매개도적원위결구말단표기법검측31례OLP화10례정상구강점막(normal oral mucosa,NOM)중림파세포조망정황;분별사용면역조화법검측조직총림파세포급CD8~+、CD4~+T세포Fas、FasL적표체.결과 OLP여NOM고유층림파세포조망솔[분별위(1.9±1.8)%、(11.5±9.0)%]차이유통계학의의(P=0.013).OLP림파세포Fas、FasL표체여NOM조상비명현증강[양성표체솔분별위52%(16/31)、71%(22/31),P치분별위0.005、0.000].OLP중CD8~+여Fas~+세포쌍양성표체솔위10%,여NOM조상비무명현승고(P=0.313),이CD8~+여FasL~+세포쌍양성표체솔[58%(3/31)]현저승고(P=0.002).CD4~+여Fas~+세포쌍양성표체솔위35%(11/31),교NOM조현저승고(P=0.031),기중망문형적표체명현승고(양성표체위8/19,P=0.019),단미란、위축형적표체무현저승고(양성표체위3/12,P=0.097).CD4~+여FasL~+표체솔위16%(5/31),여NOM조상비무명현증강(P=0.182).결론 OLP림파세포조망저하;OLP중T세포아군Fas、FasL표체불균형,CD8~+세포화위축、미란형OLP중CD4~+세포가능도일AICD,여염증적지속화진전유관;망문형OLP중부분CD4~+T세포가능경력AICD.
Objective To examine the expression of Fas and Fas ligand(FasL)in T lymphocytes of oral lichen planus(OLP)and the effects of Fas,FasL and activation-induced cell death(AICD)on OLP.Methods The oral mucosa samples from patients with OLP and nomal oral mucosa were assessed by in situ terminal deoxynucleotidyl transferase(TdT)-mediated deoxvuridine-5'-triphosphate(dUTP)-biotin nick endlabelling(TUNEL)assay for nucleosomal DNA fragmentation of apoptotic cells in infiltrating lymphocytes.Immunohistochemcial technique was used for detection of expression level of Fas and FasL.Immunohistochemcial double labeling was performed to examine the expression of Fas and FasL in CD8~+ T cells and CD4~+ T cells.Results The rate of apoptosis in infiltrating lymphocytes of OLP was(1.9±1.8)%,which was lower than that of normal oral mucosa(P=0.013).The expression of Fas and FasL were increased in lymphocytes of OLP(P=0.005 and 0.000 respectively).The positive rate of double labeled cells of CD8~+ and Fas~+ was not increased in OLP(P=0.313),and of CD8~+ and FasL~+ in OLP was higher than that of normal oral mucosa(P=0.002).The expression of double labeled cells of CD4~+ and Fas~+ in OLP was higher than that of control group(P=0.031).The expression of CD4~+ and Fas~+ T cells in reticular OLP were increased(P=0.019),and of CD4+ and FasL+ did not show remarkable change(P=0.097).Conclusions There was a low frequency of lymphocytic apoptosis.T cells,especial CD8~+ T cells in OLP and CD4~+ T cells in atrophic-erosive OLP appeared to escape from AICD,which may account for the persistense of inflammation.Some CD4~+ T cells in reticular OLP may go through AICD.
