Accolla Roberto S, Lombardo Letizia, Abdallah Rawan, Raval Goutham, Forlani Greta, Tosi Giovanna
Department of Surgical and Morphological Sciences, University of Insubria , Varese , Italy.
Front Oncol. 2014 Feb 18;4:32. doi: 10.3389/fonc.2014.00032. eCollection 2014.
Although the existence of an immune response against tumor cells is well documented, the fact that tumors take off in cancer patients indicates that neoplastic cells can circumvent this response. Over the years many investigators have described strategies to rescue the anti-tumor immune response with the aim of creating specific and long-lasting protection against the disease. When exported to human clinical settings, these strategies have revealed in most cases a very limited, if any, positive outcome. We believe that the failure is mostly due to the inadequate triggering of the CD4+ T helper (TH) cell arm of the adaptive immunity, as TH cells are necessary to trigger all the immune effector mechanisms required to eliminate tumor cells. In this review, we focus on novel strategies that by stimulating MHC class II-restricted activation of TH cells generate a specific and persistent adaptive immunity against the tumor. This point is of critical importance for both preventive and therapeutic anti-tumor vaccination protocols, because adaptive immunity with its capacity to produce specific, long-lasting protection and memory responses is indeed the final goal of vaccination. We will discuss data from our as well as other laboratories which strongly suggest that triggering a specific and persistent anti-tumor CD4+ TH cell response stably modify not only the tumor microenvironment but also tumor-dependent extratumor microenvironments by eliminating and/or reducing the blood-derived tumor infiltrating cells that may have a pro-tumor growth function such as regulatory CD4+/CD25+ T cells and myeloid-derived-suppressor cells. Within this frame, therefore, we believe that the establishment of a pro-tumor environment is not the cause but simply the consequence of the tumor strategy to primarily counteract components of the adaptive cellular immunity, particularly TH lymphocytes.
尽管针对肿瘤细胞的免疫反应的存在已有充分记录,但肿瘤在癌症患者体内发展这一事实表明,肿瘤细胞能够规避这种免疫反应。多年来,许多研究人员描述了挽救抗肿瘤免疫反应的策略,旨在建立针对该疾病的特异性和持久保护。当这些策略应用于人类临床时,在大多数情况下,其积极效果非常有限,甚至没有效果。我们认为,失败主要是由于适应性免疫的CD4 + T辅助(TH)细胞臂触发不足,因为TH细胞是触发消除肿瘤细胞所需的所有免疫效应机制所必需的。在这篇综述中,我们重点关注通过刺激MHC II类限制性TH细胞活化来产生针对肿瘤的特异性和持久适应性免疫的新策略。这一点对于预防性和治疗性抗肿瘤疫苗接种方案都至关重要,因为具有产生特异性、持久保护和记忆反应能力的适应性免疫确实是疫苗接种的最终目标。我们将讨论来自我们实验室以及其他实验室的数据,这些数据强烈表明,触发特异性和持久的抗肿瘤CD4 + TH细胞反应不仅会稳定地改变肿瘤微环境,还会通过消除和/或减少可能具有促肿瘤生长功能的血源性肿瘤浸润细胞(如调节性CD4 + / CD25 + T细胞和髓源性抑制细胞)来改变肿瘤依赖性瘤外微环境。因此,在这个框架内,我们认为促肿瘤环境的建立不是原因,而仅仅是肿瘤主要对抗适应性细胞免疫成分(特别是TH淋巴细胞)策略的结果。