Laboratory of Tumor Inflammation and Angiogenesis, Center for Cancer Biology, Flanders Institute for Biotechnology (VIB), Leuven, Belgium.
Laboratory of Tumor Inflammation and Angiogenesis, Center for Cancer Biology, Department of Oncology, KU Leuven, Leuven, Belgium.
Cancer Immunol Res. 2023 Dec 1;11(12):1611-1629. doi: 10.1158/2326-6066.CIR-22-0606.
Forkhead box P3 (Foxp3)-expressing regulatory T cells (Treg) are the guardians of controlled immune reactions and prevent the development of autoimmune diseases. However, in the tumor context, their increased number suppresses antitumor immune responses, indicating the importance of understanding the mechanisms behind their function and stability. Metabolic reprogramming can affect Foxp3 regulation and, therefore, Treg suppressive function and fitness. Here, we performed a metabolic CRISPR/Cas9 screen and pinpointed novel candidate positive and negative metabolic regulators of Foxp3. Among the positive regulators, we revealed that targeting the GDP-fucose transporter Slc35c1, and more broadly fucosylation (Fuco), in Tregs compromises their proliferation and suppressive function both in vitro and in vivo, leading to alteration of the tumor microenvironment and impaired tumor progression and protumoral immune responses. Pharmacologic inhibition of Fuco dampened tumor immunosuppression mostly by targeting Tregs, thus resulting in reduced tumor growth. In order to substantiate these findings in humans, tumoral Tregs from patients with colorectal cancer were clustered on the basis of the expression of Fuco-related genes. FucoLOW Tregs were found to exhibit a more immunogenic profile compared with FucoHIGH Tregs. Furthermore, an enrichment of a FucoLOW signature, mainly derived from Tregs, correlated with better prognosis and response to immune checkpoint blockade in melanoma patients. In conclusion, Slc35c1-dependent Fuco is able to regulate the suppressive function of Tregs, and measuring its expression in Tregs might pave the way towards a useful biomarker model for patients with cancer. See related Spotlight by Silveria and DuPage, p. 1570.
叉头框蛋白 P3(Foxp3)表达的调节性 T 细胞(Treg)是控制免疫反应的守护者,可防止自身免疫性疾病的发生。然而,在肿瘤环境中,其数量的增加会抑制抗肿瘤免疫反应,这表明了解其功能和稳定性背后的机制非常重要。代谢重编程会影响 Foxp3 的调控,从而影响 Treg 的抑制功能和适应性。在这里,我们进行了代谢 CRISPR/Cas9 筛选,并确定了 Foxp3 调控的新型候选代谢正、负调控因子。在阳性调控因子中,我们揭示了靶向 Treg 中的 GDP-岩藻糖转运蛋白 Slc35c1,以及更广泛的岩藻糖基化(Fuco),会损害 Treg 的增殖和抑制功能,无论是在体外还是体内,导致肿瘤微环境改变和肿瘤进展受损以及促进肿瘤的免疫反应。Fuco 的药理学抑制主要通过靶向 Treg 来减轻肿瘤免疫抑制,从而导致肿瘤生长减少。为了在人类中证实这些发现,我们根据 Fuco 相关基因的表达对结直肠癌患者的肿瘤 Treg 进行聚类。与 FucoHIGH Treg 相比,FucoLOW Treg 表现出更具免疫原性的特征。此外,FucoLOW 特征的富集主要来自 Treg,与黑色素瘤患者的更好预后和对免疫检查点阻断的反应相关。总之,Slc35c1 依赖性 Fuco 能够调节 Treg 的抑制功能,测量其在 Treg 中的表达可能为癌症患者开辟有用的生物标志物模型的道路。见相关的 Spotlight 由 Silveria 和 DuPage 撰写,第 1570 页。