决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:Metabolic-immune axis in the tumor microenvironment: a new strategy for prognostic assessment and precision therapy in DLBCL and FL.
弥漫大 B 细胞淋巴瘤和滤泡性淋巴瘤表现出复杂的代谢和免疫微环境,这些微环境影响疾病进展和治疗反应。
弥漫大B细胞淋巴瘤和滤泡性淋巴瘤具有复杂的代谢和免疫微环境,会影响疾病进展及治疗应答。代谢重编程,包括糖酵解、氨基酸代谢和脂质代谢,可支持肿瘤生长并抑制抗肿瘤免疫。TIL(肿瘤浸润淋巴细胞)以及PD-L1、LAG-3、TIM-3等检查点分子等免疫组分也会进一步调节预后。肿瘤代谢体积和糖酵解活性升高与疾病侵袭性增强及结局不良相关。相反,TIL密度较高往往预示更好的治疗应答。整合代谢和免疫生物标志物有助于优化风险分层和治疗策略,并凸显联合代谢抑制剂与免疫疗法以改善淋巴瘤精准医疗的潜力。
Diffuse large B-cell lymphoma and follicular lymphoma exhibit complex metabolic and immune microenvironments that influence disease progression and treatment response. Metabolic reprogramming, including glycolysis, amino acid, and lipid metabolism, supports tumor growth while suppressing anti-tumor immunity. Immune components such as tumor-infiltrating lymphocytes and checkpoint molecules (PD-L1, LAG-3, TIM-3) further modulate prognosis. Elevated tumor metabolic volume and glycolytic activity correlate with aggressive disease and poor outcomes. Conversely, high TIL density often predicts better responses. Integrating metabolic and immune biomarkers enhances risk stratification and therapeutic strategies, highlighting the potential for combined metabolic inhibitors and immunotherapies to improve precision medicine in lymphoma.
MEMBER ACCOUNT
登录成功会直接打开下一页。