Koelsch Nicholas, Manjili Masoud H
Department of Microbiology and Immunology, Virginia Commonwealth University (VCU) School of Medicine, Richmond, VA, USA.
VCU Massey Comprehensive Cancer Center, Richmond, VA, USA.
Br J Cancer. 2025 Aug 4. doi: 10.1038/s41416-025-03133-y.
The quest for a curative cancer immunotherapy remains elusive, hindered by a longstanding focus on tumor cell elimination through cytotoxic mechanisms. However, mounting evidence points to an underappreciated dimension of immune function: its capacity for tissue remodeling and homeostasis, which can shape a tumor-inhibitory microenvironment. This perspective review highlights the adaptation model of immunity, which reframes the immune response as a dual force capable of both preserving and disrupting tissue integrity. Central to this model is Signal IV, a novel pathway in which self-reactive immune cells interact with adaptation receptors (AdRs) on tissue cells through adaptation ligands (AdLs) on immune cells. This interaction activates anti-apoptotic pathways in target cells, enabling immune responses to promote tissue survival and homeostasis even in the presence of cytotoxic mediators. Crucially, the downregulation of AdRs in stromal cells, while preserved in malignant cells, creates a tumor-promoting microenvironment, whereas the reverse fosters tumor rejection. This paradigm challenges conventional approaches by shifting the focus from tumor cell destruction to restoring tissue integrity, offering a revolutionary framework for immunotherapy. By targeting the AdR-AdL axis to reprogram the tumor microenvironment, the adaptation model proposes a transformative strategy for harnessing immune responses to achieve durable cancer control.
由于长期以来专注于通过细胞毒性机制消除肿瘤细胞,治愈性癌症免疫疗法的探索仍然难以实现。然而,越来越多的证据表明免疫功能存在一个未被充分认识的维度:其组织重塑和内稳态维持能力,这可以塑造一个抑制肿瘤的微环境。这篇观点综述强调了免疫适应模型,该模型将免疫反应重新定义为一种既能维持又能破坏组织完整性的双重力量。该模型的核心是信号四(Signal IV),这是一条新的途径,其中自身反应性免疫细胞通过免疫细胞上的适应配体(AdL)与组织细胞上的适应受体(AdR)相互作用。这种相互作用激活靶细胞中的抗凋亡途径,使免疫反应即使在存在细胞毒性介质的情况下也能促进组织存活和内稳态维持。至关重要的是,基质细胞中AdR的下调,而恶性细胞中AdR则得以保留,会产生一个促进肿瘤的微环境,反之则促进肿瘤排斥。这种范式通过将重点从肿瘤细胞破坏转向恢复组织完整性,挑战了传统方法,为免疫疗法提供了一个革命性的框架。通过靶向AdR-AdL轴来重新编程肿瘤微环境,适应模型提出了一种变革性策略,以利用免疫反应实现持久的癌症控制。