摘要
目的:研究尖锐湿疣(CA)组织中朗格汉斯细胞(Langerhans’cell,LC)表面标志分子CD1a、趋化因子巨噬细胞炎性蛋白3α(MIP-3α)及黏附分子上皮细胞钙黏素(E-cadherin)mRNA表达,探讨CA局部LC改变的分子机制。方法:采用反转录(RT)-PCR法检测26例CA组织中CD1a、MIP-3α、E-cadherin的表达情况,并以10名正常人包皮组织作为对照。结果:①与正常对照组(0.7444±0.3667)相比,CA组织中CD1a mRNA表达(0.4066±0.2671)显著降低(P<0.01),MIP-3α mRNA表达(0.3181±0.1632)低于正常对照组(0.6163±0.1939)(P<0.01),E-cadherin mRNA表达(0.1737±0.1083)较正常对照组(0.3786±0.1460)显著降低(P<0.01)。②CD1a和MIP-3α分子mRNA的表达呈正相关(r=0.9533,P<0.01),CD1a和E-cadherin分子mRNA的表达也呈正相关(r=0.8381,P<0.05)。结论:CA组织中存在LC缺失和抗原提呈功能下降,LC的减少可能与表皮MIP-3α表达下降,进而导致LC前体细胞难以到达表皮有关,还可能与E-cadherin表达下降导致LC在表皮内难以滞留有关。
Objective： To explore the molecular mechanism of Langerhans＇ cells （LC） alteration in condyloma accuminatum by detecting CD1a, MIP-3α and E-cadherin mRNAs in situ. Methods： CD1a, MIP-3α and E-cadherin mRNAs were measured by reverse transcriptaion （RT） and polymerase chain reaction （PCR） respectively in 26 condyloma accuminatum （CA） and 10 normal controls. Results： Compared with normal tissues, expressions of CD1a, MIP-3α and E-cadherin were significantly down-regulated in CA （P〈 0.01）. The positive correlations between CDla and MIP-3α （r = 0.953 3, P〈 0.01）, CD1a and E-cadherin（r = 0.8381, P〈 0.05）were observed, respectively. Conclusion： CA is characterized by decreased LC density and reduced function of antigen presenting. The depletion of LC may be due to the less expression of MIP-3α which hampered the LC precursor migrating to the epidermis and the deficiency of LC retention in the local because of the decreased expression of E-cadherin as well
出处
《临床皮肤科杂志》
CAS
CSCD
北大核心
2008年第5期287-289,共3页
Journal of Clinical Dermatology
基金
国家自然科学基金预研项目资助(KJ0790297)
