LNCaP公司
细胞因子
增生
癌症研究
免疫系统
前列腺
热休克蛋白
肿瘤坏死因子α
下调和上调
免疫疗法
热疗
医学
抗原
病理
生物
免疫学
内科学
癌症
生物化学
基因
作者
Gero Kramer,Georg Steiner,Marion Gröbl,Kristian Hrachowitz,Franz Reithmayr,Ljubomir Paucz,Martin Newman,Stephan Madersbacher,Doris Gruber,Martin Susani,Michael Marberger
出处
期刊:The Prostate
[Wiley]
日期:2003-11-17
卷期号:58 (2): 109-120
被引量:72
摘要
To investigate the possibilities offered by high intensity focused ultrasound (HIFU) in the field of tumor vaccination, we analyzed how prostatic cancer (CaP) cells react towards heat treatment and whether increased access to CaP cells by the immune system would be the result.Heat/stress response of CaP cells in situ and of CaP cell lines was analyzed by immunohistochemistry, Western blotting, and Atlas array. A heat-induced change in immune recognition was analyzed functionally using human T-helper (Th)1 and Th2-cytokine release with tumor infiltrating T-lymphocytes (TIL) as responder and autologous CaP cells either heated or untreated as stimulator cells.Transcription of 68 out of 500 genes was upregulated by sublethal heat in LNCaP and PC3 cells. Significantly upregulated stress protein (SP) expression (HSP-72, -73, GRP-75, -78) was seen at the border zone of HIFU treatment. Remarkably, even untreated benign prostatic hyperplasia (BPH) specimens revealed relative overexpression of heat shock protein (HSP)-72, -73 and glucose regulated protein (GRP)-75, -78. Heated CaP cells increased Th1-cytokine (IL-2, IFN-gamma, TNF-alpha) release but decreased Th2-cytokine (IL-4, -5, -10) release of TIL.HIFU treatment may alter the presentation of prostate tissue and tumor antigens and this presentation is most likely stimulatory. HSP-72/73 overexpression in untreated BPH may suggest a mechanism by which BPH can incite inflammation.
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