美国纪念斯隆凯特琳癌症中心的研究人员确定了导致癌症免疫疗法中T细胞耗尽的关键机制。1研究发现，信号分子MEK驱动了这一耗尽过程，而阻断MEK可以降低T细胞的能量需求，使其保存更多能量、存活更长时间，从而延长免疫疗法的有效性。1该研究已于2026年6月发表在《免疫学》期刊上。1
研究团队发现，耗尽的T细胞并非功能低下而是代谢活跃的。1主要作者Tanmana Mitra博士表示："T细胞耗尽不是简单的功能丧失，而是反映这些细胞被要求做的事情与可用能量之间的不平衡。"1通过阻断MEK信号，T细胞消耗更少能量的同时增殖更多，使其能够保存更多能量并存活更长时间。1
这一发现的临床转化前景广阔。1共同研究者Santosha Vardhana博士指出："FDA批准的MEK抑制剂已经可用，因此这种方法可以在没有多大延迟的情况下在人体中进行测试。"1研究表明，MEK抑制剂可能对肿瘤较大或免疫细胞较少的患者特别有益。1
Researchers at Memorial Sloan Kettering Cancer Center have identified a molecular mechanism underlying a critical limitation of cancer immunotherapy: the progressive exhaustion of T cells.1 The team discovered that the signaling molecule MEK drives this exhaustion process, and blocking it can restore T cell function and extend the effectiveness of treatment.1
According to the study published in Immunity in June 2026, exhausted T cells are not simply dysfunctional but rather face an energy imbalance between their metabolic demands and available resources.1 Dr. Tanmana Mitra explained: "T cell exhaustion is not simply a loss of function, but rather reflects an imbalance between what these cells are being asked to do and the energy available to them."1 The research revealed that contrary to previous assumptions, exhausted T cells maintain high metabolic activity; blocking MEK allows them to consume less energy while proliferating more effectively.1
The practical implications of this discovery are significant because FDA-approved MEK inhibitors are already available for clinical use.1 Dr. Santosha Vardhana noted: "FDA-approved MEK inhibitors are already available, so this approach can be tested in humans without much delay."1 The researchers suggest that this intervention may prove particularly beneficial for patients with larger tumors or those with fewer immune cells available for treatment.1
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