共刺激分子在宫颈癌组织中的表达

目的 研究宫颈癌组织中癌细胞中的共刺激分子Ｂ７．１、Ｂ７．２、细胞间粘附因子－Ｉ（ＩＣＡＭ－１）及主要组织相容性抗原（ＭＨＣ）Ｉ、Ⅱ类分子表达，以揭示人体肿瘤的逃逸机制。方法 利用免疫组织化学技术，观察了４２例人宫颈癌组织中Ｂ７．１、Ｂ７．２、ＩＣＡＭ－１的表达，观察了３６例ＭＨＣＩ、Ⅱ类抗原的表达；利用原位杂交技术观察了２０例人宫颈癌组织中Ｂ７．１、Ｂ７．２和ＩＣＡＭ－１的ｍＲＮＡ表达。结果 在

An insitu study on immunostimulatory molecules in cancer cells within the cervical carcinomatissues

OBJECTIVE: To explore the immune escape mechanism by investigating the expression of B7.1, B7.2, ICAM-1 and MHCI, MHCII Ag in the cancer cells of cervical carcinoma. METHODS: The expressions of B7.1, B7.2 and ICAM-1, together with MHCI and IIAg were analyzed in tumor cells and interstitial cells of human cervical carcinoma with immunohistochemistry technique. The mRNA expressions of B7.1, B7.2 and ICAM-1 were observed by in situ hybridization. RESULTS: Out of the 42 fresh specimens analyzed with immunohistochemistry, the tumor cells expressed B7.1 Ag and ICAM-1 molecules in 22 and 27 specimens respectively, but not expressed B7.2; B7.1(+), B7.2(+) and ICAM-1(+) dendritic cells and lymphocytes were scattered more or less in the parenchyma and interstitum. Among the 37 cases studied for MHC Ag expression, the tumor cells expressed MHCI Ag and MHCIIAg in 32 and 4 cases respectively. No matter whether the tumor cells expressed MHCIIAg or not, MHCIIAg(+) dendritic cells were observed in the nests and the interstitial. When the same section staind for identifying, B7.1, B7.2 and MHCIIAg expressions was compared, by and large, the MHCIIAg(+) dendritic cells were always more numerous than B7.1, B7.1(+) or B7.2(+) ones. As for the 20 specimens inspected with in situ hybridization, the tumor cells in 11 and 12 cases expressed B7.1 mRNA and ICAM-1 mRNA respectively; Infiltrating dendritic cells and lymphocytes expressed B7.1 mRNA, B7.2 mRNA and ICAM-1 mRNA. CONCLUSION: Tumor cells in most cervical carcinomas have the necessary elements for presenting antigen and evoking T lymphocytes activation, and there are a lot of dendritic cells infiltrated in the tumor tissues. These findings indicate that the mechanism for tumor escape may be attributed to the post-antigen presentation events.