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標籤： T細胞
賓夕法尼亞大學的研究人員報告說，p53 蛋白的變體可能會增加嵌合抗原受體 （CAR） T 細胞的有效性**。
researchers at the university of pennsylvania report a variant of the p53 protein may improve the effectiveness of chimeric antigen receptor (car) t cell therapy.
研究結果發表在《美國國家科學院院刊》上，作者是病理學和檢驗醫學系免疫學系的Richard W.由Vague教授領導的Carl June博士，他是佩雷爾曼醫學院細胞免疫中心**主任和賓夕法尼亞大學帕克癌症免疫研究所**主任。
the findings are published in the proceedings of the national academy of sciences and led by carl june, md, the richard w. vague professor in immunotherapy in the department of pathology and laboratory medicine, director of the center for cellular immunotherapies at the perelman school of medicine, and director of the parker institute for cancer immunotherapy at the university of pennsylvania.
“CAR T細胞是血癌的一種轉化形式，受到T細胞功能障礙的限制，特別是在慢性淋巴細胞白血病（CLL）中，”研究人員寫道。 ”。我們的研究揭示了人類和猿特異性 p53 亞型 δ133p53 在增強 CAR T 細胞的作用中的關鍵作用**。 δ133P53A在CAR T淋巴細胞中的表達可以提高其代謝穩定性，使其具有優越的抗腫瘤功能，特別是在高腫瘤負荷條件下。 ”
car t cell therapy, a transformative treatment for blood cancers, is limited by t cell dysfunction, especially in chronic lymphocytic leukemia (cll),”the researchers wrote. “our study reveals a pivotal role for the human and great ape-specific p53 isoform, δ133p53α, in enhancing the therapeutic efficacy of car t cells. expressing δ133p53α in car t cells improves their metabolic robustness, enabling superior antitumor function particularly under high tumor burden conditions.”
June及其同事靶向p53蛋白變體δ133p53，其在人類T細胞中的表達隨著年齡的增長而降低。
june and colleagues targeted the p53 protein variant δ133p53α, which decreases in expression with age in human t cells.
在臨床試驗中，133p53 的持續表達改善了由健康正常供體和 CAR T 細胞難治的 CLL 患者**製成的 CAR T 淋巴細胞的抗腫瘤功能。 δ133p53在CAR T細胞中的表達可增強細胞代謝功能並增強抗腫瘤活性，尤其是在腫瘤負荷高的條件下。 在營養限制條件下，表達δ133P53的CAR T細胞不僅清除了更多的腫瘤，而且增殖了更多，部分原因是關鍵生物合成過程的增強和線粒體功能的改善。
continual expression of δ133p53α improved the antitumor function of car t cells manufactured from both healthy normal donors and from people with cll who failed to respond to car t cell therapy during clinical trials. expressing δ133p53α in car t cells enhanced the cells’ metabolic function, boosting antitumor activity, especially under conditions of high tumor burden. under nutrient-limiting conditions, car t cells expressing δ133p53α not only cleared significantly more tumor but also displayed increased proliferation, partly due to the enhancement of key biosynthetic processes and improved mitochondrial function.
這些發現指出了p53訊號轉導網路作為延長CAR T細胞反應調節劑的重要作用，並為抗癌T細胞的利用提供了新的途徑。
the findings point to the significant role of the p53 signaling network as a regulator of prolonged car t cell responses and provides new **enues of therapies that harness cancer-fighting t cell
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