Sharpe J C, Abel P D, Gilbertson J A, Brawn P, Foster C S
Department of Histopathology, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Br J Urol. 1994 Nov;74(5):609-16. doi: 10.1111/j.1464-410x.1994.tb09193.x.
To determine whether human prostatic carcinoma cells express Class I and/or Class II major histocompatibility complex (MHC) determinants and whether they might thus be immune-competent targets for cell-mediated cytotoxicity.
Immunohistochemistry, performed both before and after neuraminidase digestion, was employed to compare 13 benign prostatic hyperplasias with 42 primary and 44 metastatic prostatic carcinomas obtained from the United Kingdom and from the United States of America. Expression of beta 2-microglobulin was used as the marker of Class I and HLA-DR as the marker of Class II expression.
Before desialylation, Class I MHC determinants were expressed in all of the benign hyperplasias, in 26% of primary carcinomas and in 14% of lymph node metastases. Cells expressing Class II determinants were identified in 69% of benign hyperplasias and in 2% of primary carcinomas, but in none of the lymph node metastases. After desialylation. Class I determinants were expressed in 100% of benign hyperplasias. 59% of primary carcinomas and 34% of the lymph node metastases. Class II determinants were expressed in 100% of benign hyperplasias, but only 19% of primary carcinomas and 5% of the lymph node metastases. While more than 50% of epithelial cells in each of the benign hyperplasias expressed MHCs, < 5% of the tumour cell populations in the positive malignant tissues (primary and metastatic) expressed MHCs, even after neuraminidase digestion. No correlation was found between expression of Class I or Class II MHC and Gleason morphological grade.
Failure to express Class I and/or Class II MHC determinants is a common feature of the majority of human prostatic carcinoma cells. Absence of these recognition molecules may be associated with avoidance of immune-surveillance and contribute to the metastatic dissemination of this malignancy.
确定人类前列腺癌细胞是否表达I类和/或II类主要组织相容性复合体(MHC)决定簇,以及它们是否可能因此成为细胞介导的细胞毒性的免疫活性靶点。
采用免疫组织化学方法,在神经氨酸酶消化前后进行检测,比较来自英国和美国的13例良性前列腺增生、42例原发性前列腺癌和44例转移性前列腺癌。β2-微球蛋白的表达用作I类标志物,HLA-DR用作II类表达的标志物。
在去唾液酸化之前,I类MHC决定簇在所有良性增生中均有表达,在26%的原发性癌和14%的淋巴结转移中表达。在69%的良性增生和2%的原发性癌中发现了表达II类决定簇的细胞,但在淋巴结转移中均未发现。去唾液酸化后,I类决定簇在100%的良性增生、59%的原发性癌和34%的淋巴结转移中表达。II类决定簇在100%的良性增生中表达,但仅在19%的原发性癌和5%的淋巴结转移中表达。虽然每个良性增生中超过50%的上皮细胞表达MHC,但即使在神经氨酸酶消化后,阳性恶性组织(原发性和转移性)中<5%的肿瘤细胞群体表达MHC。未发现I类或II类MHC的表达与Gleason形态学分级之间存在相关性。
大多数人类前列腺癌细胞的一个共同特征是未能表达I类和/或II类MHC决定簇。这些识别分子的缺失可能与免疫监视的逃避有关,并有助于这种恶性肿瘤的转移扩散。