Tong Alex W, Stone Marvin J
Cancer Immunology Research Laboratory, Baylor Sammons Cancer Center, Baylor University Medical Center, Dallas, Texas 75246, USA.
Cancer Gene Ther. 2003 Jan;10(1):1-13. doi: 10.1038/sj.cgt.7700527.
CD40, a member of the tumor necrosis factor receptor (TNF-R) family, is a surface receptor best known for its capacity to initiate multifaceted activation signals in normal B cells and dendritic cells (DCs). CD40-related treatment approaches have been considered for the experimental therapy of human leukemias, lymphomas, and multiple myeloma, based on findings that CD40 binding by its natural ligand (CD40L), CD154, led to growth modulation of malignant B cells. Recent studies also exploited the selective expression of the CD40 receptor on human epithelial and mesenchymal tumors but not on most normal, nonproliferating epithelial tissues. Ligation of CD40 on human breast, ovarian, cervical, bladder, non small cell lung, and squamous epithelial carcinoma cells was found to produce a direct growth-inhibitory effect through cell cycle blockage and/or apoptotic induction with no overt side effects on their normal counterparts. CD154 treatment also heightened tumor rejection immune responses through DC activation, and by increasing tumor immunogenicity through up-regulation of costimulatory molecule expression and cytokine production of epithelial cancer cells. These immunopotentiating features can produce a "bystander effect" through which the CD40-negative tumor subset is eliminated by activated tumor-reactive cytotoxic T cells. However, the potential risk of systemic inflammation and autoimmune consequences remains a concern for systemic CD154-based experimental therapy. The promise of CD154 as a tumor therapeutic agent to directly modulate tumor cell growth, and indirectly activate antitumor immune response, may depend on selective and/or restricted CD154 expression within the tumor microenvironment. This may be achieved by inoculating cancer vaccines of autologous cancer cells that have been transduced ex vivo with CD154, as documented by recently clinical trials. This review summarizes recent findings on CD154 recombinant protein- and gene therapy-based tumor treatment approaches, and examines our understanding of the multifaceted molecular mechanisms of CD154-CD40 interactions.
CD40是肿瘤坏死因子受体(TNF-R)家族的成员之一,是一种表面受体,因其能够在正常B细胞和树突状细胞(DC)中引发多方面的激活信号而广为人知。基于CD40与其天然配体(CD40L)CD154结合可导致恶性B细胞生长调节的研究结果,CD40相关的治疗方法已被考虑用于人类白血病、淋巴瘤和多发性骨髓瘤的实验性治疗。最近的研究还利用了CD40受体在人类上皮和间充质肿瘤上的选择性表达,而在大多数正常的、非增殖性上皮组织上则不表达。研究发现,在人乳腺癌、卵巢癌、宫颈癌、膀胱癌、非小细胞肺癌和鳞状上皮癌细胞上连接CD40可通过细胞周期阻滞和/或诱导凋亡产生直接的生长抑制作用,而对其正常对应物没有明显的副作用。CD154治疗还通过DC激活增强肿瘤排斥免疫反应,并通过上调共刺激分子表达和上皮癌细胞的细胞因子产生来增加肿瘤免疫原性。这些免疫增强特性可产生“旁观者效应”,通过该效应,活化的肿瘤反应性细胞毒性T细胞可消除CD40阴性肿瘤亚群。然而,基于全身性CD154的实验性治疗,全身炎症和自身免疫后果的潜在风险仍然是一个问题。CD154作为一种肿瘤治疗剂直接调节肿瘤细胞生长并间接激活抗肿瘤免疫反应的前景,可能取决于肿瘤微环境中CD154的选择性和/或限制性表达。这可以通过接种经CD154体外转导的自体癌细胞癌症疫苗来实现,最近的临床试验已证明这一点。本综述总结了基于CD154重组蛋白和基因治疗的肿瘤治疗方法的最新研究结果,并探讨了我们对CD154-CD40相互作用多方面分子机制的理解。