Vidas Zeljko
Department of Urology, "Merkur" University Hospital, Zagreb, Croatia.
Coll Antropol. 2010 Jun;34(2):779-83.
Toll-like receptors are key players in initiation of innate immune response of the host. In addition to innate immunity they can also induce adaptive immune responses. The concept that inflammation can promote chronic prostatic diseases, such as benign prostatic hyperplasia or prostate carcinoma is supported by several new findings. Epidemiological data have correlated prostatitis with an increased risk of prostate cancer, while PCR-based analyses of bacterial colonization in prostate cancer specimens and normal prostate tissue showed high correlation of bacterial colonization and chronic inflammation with a diagnosis of prostate carcinoma. Even evidence from genetic studies support the hypothesis that prostate inflammation may be a cause of prostate cancer. From these points of view identification of factors, such as SNPs in TLR genes, associated with risk for prostate carcinoma development seems reasonable. Consequently, there are many investigations showing the connection between SNPs in TLR genes and pronounced susceptibility to different diseases. In this article we review the key findings about the genetic variability of TLR genes and prostate cancer risk.
Toll样受体是宿主先天免疫反应启动中的关键因素。除先天免疫外，它们还可诱导适应性免疫反应。炎症可促进慢性前列腺疾病（如良性前列腺增生或前列腺癌）这一概念得到了多项新发现的支持。流行病学数据已将前列腺炎与前列腺癌风险增加相关联，而基于聚合酶链反应（PCR）对前列腺癌标本和正常前列腺组织中细菌定植的分析表明，细菌定植和慢性炎症与前列腺癌诊断高度相关。甚至来自基因研究的证据也支持前列腺炎症可能是前列腺癌病因这一假说。从这些观点来看，鉴定与前列腺癌发生风险相关的因素（如TLR基因中的单核苷酸多态性（SNP））似乎是合理的。因此，有许多研究表明TLR基因中的SNP与对不同疾病的明显易感性之间存在关联。在本文中，我们综述了关于TLR基因遗传变异性与前列腺癌风险的关键发现。
