一项研究发现，在多数动物研究机构小鼠生活的地方的温度可能扭曲癌症免疫疗法研究的结果。小鼠天然地寻找温暖的巢环境从而让产热代谢活动的能量开支最小化，并且已知健康的小鼠喜爱30到31摄氏度的环境温度。
然而，大多数动物研究机构的实验室小鼠生活在20到26摄氏度的环境中，这部分是为了减少对笼子清洁的要求并且增加技术人员的舒适度。尽管低于最优的温度导致了轻微的冷压力，实验室小鼠通常维持了正常的体温。
为了确定这种温度不一致是否可能影响疾病病程，Elizabeth Repasky及其同事比较了生活在22-23摄氏度或30-31摄氏度的几个常见癌症小鼠模型的肿瘤形成、生长率和转移。这组作者报告说，生活在30摄氏度的小鼠的4种不同类型的移植肿瘤比生活在22度的小鼠的肿瘤生长更缓慢，即便这两组小鼠都维持了正常体温。类似地，致癌物引发的肿瘤和一个移植的乳腺肿瘤向肺转移在更高温度生活的小鼠身上得到了更好的控制。
这组作者报告说，在30摄氏度的这种改善的肿瘤生长控制可能是被适应性免疫应答的相应增加调控的，其证据是杀手淋巴T细胞在肿瘤内部增加，而在免疫抑制细胞内减少。这组作者提出，由于冷压力可能转移用于产热的能量，并且抑制抗癌免疫应答，环境温度可能影响实验室小鼠对实验性癌症免疫疗法的响应。（生物谷Bioon.com）
生物谷推荐的英文摘要
Proceedings of the National Academy of the Sciences of the United States of America doi: 10.1073/pnas.1304291110
Baseline tumor growth and immune control in laboratory mice are significantly influenced by subthermoneutral housing temperature
Kathleen M. Kokolusa，1， Maegan L. Capitanoa，1， Chen-Ting Leea， Jason W.-L. Enga， Jeremy D. Waighta， Bonnie L. Hylandera， Sandra Sextonb， Chi-Chen Hongc， Christopher J. Gordond， Scott I. Abramsa， and Elizabeth A. Repaskya，2
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.
