Macroautophagy (hereafter autophagy) degrades and recycles intracellular components to sustain metabolism and survival during starvation. Host autophagy promotes tumor growth by providing essential tumor nutrients. Autophagy also regulates immune cell homeostasis and function and suppresses inflammation. Although host autophagy does not promote a T-cell antitumor immune response in tumors with low tumor mutational burden (TMB), whether this was the case in tumors with high TMB was not known. Here we show that autophagy, especially in the liver, promotes tumor immune tolerance by enabling regulatory T-cell function and limiting stimulator of interferon genes, T-cell response and interferon-γ, which enables growth of high-TMB tumors. We have designated this as hepatic autophagy immune tolerance. Autophagy thereby promotes tumor growth through both metabolic and immune mechanisms depending on mutational load and autophagy inhibition is an effective means to promote an antitumor T-cell response in high-TMB tumors.

巨自噬（以下简称自噬）降解和回收细胞内成分，以在饥饿期间维持新陈代谢和生存。宿主自噬通过提供必需的肿瘤营养物质来促进肿瘤生长。自噬还调节免疫细胞稳态和功能并抑制炎症。尽管宿主自噬不会在低肿瘤突变负荷 (TMB) 的肿瘤中促进 T 细胞抗肿瘤免疫反应，但在高 TMB 的肿瘤中是否存在这种情况尚不清楚。在这里，我们表明自噬，特别是在肝脏中，通过启用调节性 T 细胞功能和限制干扰素基因、T 细胞反应和干扰素-γ 的刺激物来促进肿瘤免疫耐受，从而促进高 TMB 肿瘤的生长。我们将其命名为肝自噬免疫耐受。