2013年11月19日訊 /生物谷BIOON/--低溫會讓機體進入應激狀態(tài),，機體要提高代謝率以維持體溫,。持續(xù)低溫會讓細胞不能正常工作,。近期發(fā)表在PNAS雜志上的文章稱羅茲韋爾帕克癌癥研究中心Elizabeth Repasky博士研究組又發(fā)現(xiàn)了一個低溫的害處：低溫能夠改變癌細胞的生長和擴散的方式,。該研究對癌癥治療和癌癥基礎研究都有重要意義。
Repasky博士發(fā)現(xiàn)生活在相對低溫（22℃）的小鼠比生活在適宜溫度（30℃）的小鼠癌細胞生長會更快,，更有侵略性,。寒冷環(huán)境會增加多種類型腫瘤的生長速度,，如乳腺癌，皮膚癌,，結腸癌,，胰腺癌等。
而小鼠在患癌癥之前的環(huán)境對癌癥發(fā)展進程沒有影響,。在癌癥形成后,，寒冷才會讓癌細胞生長更快。
機體主要通過T細胞來識別并摧毀癌細胞,。而癌細胞會通過產生抑制T細胞的信號來對抗T細胞的攻擊,。這個戰(zhàn)役將抑制持續(xù)下去，直到一方勝利,。臨床上很多的抗癌療法都是讓戰(zhàn)役朝著對免疫系統(tǒng)有利的方向進行,。
寒冷和溫度舒適的小鼠有相同數(shù)量的攻擊癌細胞的T細胞。但是溫度舒適環(huán)境的小鼠體內的T細胞尋找癌細胞能力更強,，攻擊性也更好,。T細胞分泌抗癌物質也更多。
而寒冷環(huán)境的小鼠體內有更多的抑制免疫反應的細胞,，寒冷環(huán)境會讓機體適應腫瘤而不是攻擊腫瘤,。（生物谷Bioon.com）
doi: 10.1073/pnas.1304291110
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Baseline tumor growth and immune control in laboratory mice are significantly influenced by subthermoneutral housing temperature
Baseline tumor growth and immune control in laboratory mice are significantly influenced by subthermoneutral housing temperature
We show here that fundamental aspects of antitumor immunity in mice are significantly influenced by ambient housing temperature. Standard housing temperature for laboratory mice in research facilities is mandated to be between 20–26 °C; however, these subthermoneutral temperatures cause mild chronic cold stress, activating thermogenesis to maintain normal body temperature. When stress is alleviated by housing at thermoneutral ambient temperature (30–31 °C), we observe a striking reduction in tumor formation, growth rate and metastasis. This improved control of tumor growth is dependent upon the adaptive immune system. We observe significantly increased numbers of antigen-specific CD8+ T lymphocytes and CD8+ T cells with an activated phenotype in the tumor microenvironment at thermoneutrality. At the same time there is a significant reduction in numbers of immunosuppressive MDSCs and regulatory T lymphocytes. Notably, in temperature preference studies, tumor-bearing mice select a higher ambient temperature than non-tumor-bearing mice, suggesting that tumor-bearing mice experience a greater degree of cold-stress. Overall, our data raise the hypothesis that suppression of antitumor immunity is an outcome of cold stress-induced thermogenesis. Therefore, the common approach of studying immunity against tumors in mice housed only at standard room temperature may be limiting our understanding of the full potential of the antitumor immune response.
