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表观遗传增强的 PDT 诱导比标准 PDT 更高水平的多种外在途径凋亡因子,导致皮肤 T 细胞淋巴瘤的外在和整体凋亡增加。

Epigenetically Enhanced PDT Induces Significantly Higher Levels of Multiple Extrinsic Pathway Apoptotic Factors than Standard PDT, Resulting in Greater Extrinsic and Overall Apoptosis of Cutaneous T-cell Lymphoma.

机构信息

Department of Dermatology, University of Wisconsin, Madison, WI.

Department of Dermatology, Stanford University, Stanford, CA.

出版信息

Photochem Photobiol. 2018 Sep;94(5):1058-1065. doi: 10.1111/php.12925. Epub 2018 May 20.

Abstract

Aminolevulinate-based photodynamic therapy (ALA-PDT) selectively eliminates diseased tissues primarily through the induction of intrinsic apoptotic pathway. ALA-PDT is a first-line therapy for actinic keratosis, however, it is less effective for cutaneous T-cell lymphoma (CTCL). We have previously demonstrated that the resistance of CTCL to apoptosis correlates with decreased expression of death receptors such as FAS, and that methotrexate functions as an epigenetic regulator that reestablishes the susceptibility of CTCL to extrinsic pathway apoptosis. We showed previously that MTX augments the effectiveness of PDT by sensitizing cells to apoptosis by induction of apoptotic factors, a process we call "epigenetically enhanced" PDT (ePDT). Here, in CTCL cell lines, leukemic CTCL cells, and normal blood T cells, we analyzed multiple components of the FAS, TRAIL, and TNF families using multispectral imaging of immunostained cytopreparations, a quantitative technique with five-fold greater sensitivity than standard immunocytology. ePDT induced significantly greater FAS, FASL, TRAIL-R1 & -R2, and TNFα levels than standard PDT. This correlated with significantly greater induction of extrinsic pathway apoptosis and/or overall apoptosis in all CTCL samples. There was no appreciable effect on normal T cells. These data set the stage for clinical trials of ePDT as a novel localized treatment of CTCL.

摘要

基于氨基酮戊酸的光动力疗法(ALA-PDT)主要通过诱导内在凋亡途径选择性地消除病变组织。ALA-PDT 是光化性角化病的一线治疗方法,然而,对于皮肤 T 细胞淋巴瘤(CTCL)的疗效较低。我们之前已经证明,CTCL 对细胞凋亡的抵抗与死亡受体(如 FAS)的表达减少有关,并且甲氨蝶呤作为一种表观遗传调节剂,可重新建立 CTCL 对外源途径细胞凋亡的敏感性。我们之前已经表明,MTX 通过诱导凋亡因子使细胞对细胞凋亡敏感,从而增强 PDT 的有效性,这一过程我们称之为“表观遗传增强 PDT(ePDT)”。在这里,在 CTCL 细胞系、白血病 CTCL 细胞和正常血液 T 细胞中,我们使用免疫细胞化学染色的细胞涂片的多光谱成像分析了 FAS、TRAIL 和 TNF 家族的多个成分,这是一种比标准免疫细胞化学灵敏五倍的定量技术。ePDT 诱导的 FAS、FASL、TRAIL-R1 和 -R2 以及 TNFα 水平明显高于标准 PDT。这与所有 CTCL 样本中外源途径细胞凋亡和/或总细胞凋亡的诱导显著增加相关。对正常 T 细胞没有明显影响。这些数据为 ePDT 作为 CTCL 的新型局部治疗的临床试验奠定了基础。

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