Wysocka Maria, Benoit Bernice M, Newton Sarah, Azzoni Livio, Montaner Luis J, Rook Alain H
Department of Dermatology, University of Pennsylvania, 245 CRB, 415 Curie Blvd, Philadelphia, PA 19104, USA.
Blood. 2004 Dec 15;104(13):4142-9. doi: 10.1182/blood-2004-03-1190. Epub 2004 Aug 24.
Patients with advanced cutaneous T-cell lymphoma (CTCL) exhibit profound defects in cell-mediated immunity. Host immune functions appear to play an integral role in mediating disease-controlling responses in CTCL, therefore we investigated the effects of synthetic oligode-oxynucleotides with CpG motifs (CpG ODN), which have been recognized as immune stimulatory by virtue of activation of dendritic cells (DCs) following binding to Toll-like receptor (TLR) 9. Peripheral blood mononuclear cells (PBMCs) from patients with advanced CTCL (erythroderma with circulating malignant T cells) and healthy volunteers were cultured with either CpG-A or CpG-B ODN. Patients' PBMCs exhibited marked induction of interferon-alpha (IFN-alpha) release following culture with CpG-A. Similarly significant activation of NK cells and CD8 T cells occurred as assessed by up-modulation of CD69 expression and by natural killer lytic activity. Nevertheless, the PBMCs of patients exhibited blunted responses to CpG-A compared to healthy volunteers. In such cases, IL-15 was capable of producing levels of NK activation that were superior to CpG-A, while the combined effects of CpG-A plus IL-15 induced maximal activation of NK cells and further enhanced activation of CD8 T cells. These findings have important implications for the potential enhancement of antitumor immunity among patients with advanced CTCL.
晚期皮肤T细胞淋巴瘤(CTCL)患者表现出细胞介导免疫的严重缺陷。宿主免疫功能似乎在介导CTCL的疾病控制反应中起着不可或缺的作用,因此我们研究了具有CpG基序的合成寡脱氧核苷酸(CpG ODN)的作用,由于其与Toll样受体(TLR)9结合后激活树突状细胞(DC),已被认为具有免疫刺激作用。将晚期CTCL患者(红皮病伴循环恶性T细胞)和健康志愿者的外周血单个核细胞(PBMC)与CpG-A或CpG-B ODN一起培养。患者的PBMC与CpG-A培养后,干扰素-α(IFN-α)释放明显诱导。通过CD69表达上调和自然杀伤细胞溶解活性评估,NK细胞和CD8 T细胞也发生了类似的显著激活。然而,与健康志愿者相比,患者的PBMC对CpG-A的反应减弱。在这种情况下,IL-15能够产生优于CpG-A的NK激活水平,而CpG-A加IL-15的联合作用诱导了NK细胞的最大激活,并进一步增强了CD8 T细胞的激活。这些发现对晚期CTCL患者抗肿瘤免疫的潜在增强具有重要意义。