
劍橋大學與奧勒岡健康與科學大學團隊發現癌細胞逃避免疫追殺的新機制,有望改善免疫治療反應不佳問題。
英國劍橋大學與美國奧勒岡健康與科學大學團隊在《Science》發表研究指出,癌細胞會釋放PRDX1蛋白消耗活性氧,使免疫T細胞失去啟動攻擊的訊號。此發現有望為癌症免疫治療提供新方向,相關研究目前處於臨床前階段。
AI-generated summary
科學家發現腫瘤能釋放天然物質讓免疫細胞失去攻擊能力,揭露癌細胞逃避免疫追殺的新機制。
T細胞是人體免疫系統中負責辨識及攻擊異常細胞的重要角色。最新研究發現,癌細胞可能透過釋放PRDX1蛋白,干擾T細胞啟動攻擊的過程;示意圖。
人體免疫系統原本會辨識並攻擊癌細胞,但科學家發現,腫瘤竟能釋放一種天然物質,讓免疫細胞失去攻擊能力,替自己爭取生存空間。這項研究揭露癌細胞逃避免疫追殺的新機制,也為改善部分癌症患者對免疫治療反應不佳的問題,提供新的研究方向。
科學新聞網站《ScienceDaily》報導,這項研究由英國劍橋大學及美國奧勒岡健康與科學大學團隊進行,成果刊登於《Science》期刊。研究發現,癌細胞會釋放一種名為PRDX1的天然抗氧化蛋白,清除周圍環境中的特定物質,讓免疫細胞難以啟動攻擊。
這裡的關鍵是活性氧。活性氧常被認為會傷害細胞,但免疫系統中的T細胞也需要適量活性氧,才能啟動攻擊癌細胞的功能。研究發現,腫瘤釋放PRDX1後,會消耗這些活性氧,使T細胞失去啟動攻擊所需的訊號。
研究團隊利用基因編輯技術,讓小鼠癌細胞無法製造PRDX1。實驗發現,失去這種蛋白後,免疫細胞活性增加,腫瘤生長也受到抑制。
研究人員接著檢查人類癌細胞及腫瘤資料,在數千個腫瘤的基因資料,以及病人手術切除腫瘤後取得的組織液中,也找到支持這項機制的證據。
研究團隊進一步測試阻斷PRDX1對免疫治療的影響。在實驗模型中,部分原本對免疫療法反應不佳的腫瘤,在破壞這項防禦機制後,開始對治療產生反應。
研究人員表示,研究發現癌細胞會利用這種方式關閉免疫系統,阻斷相關機制後,部分原本對免疫治療沒有反應的腫瘤,開始出現治療反應。
這項發現也讓研究人員重新檢視抗氧化物的作用。活性氧雖然可能傷害細胞,卻也是免疫細胞啟動攻擊的重要訊號。研究人員認為,未來或可探索利用促氧化物質,協助T細胞恢復攻擊腫瘤的能力。
不過,這項研究目前仍處於臨床前階段。研究人員雖在人類腫瘤樣本中找到相關機制,但阻斷PRDX1能否應用於癌症治療,以及安全性與效果如何,仍有待進一步研究。

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