Abstract：
The mammalian body possesses remarkable adaptability to cold exposure, involving intricate adjustments in cellular metabolism, ultimately leading to thermogenesis. However, cold-induced stress can impact immune response, primarily through noradrenaline-mediated pathways. In our study, we utilized a rat model subjected to short-term or long-term mild cold exposure to investigate systemic immune response during the cold acclimation. To provide human relevance, we included a group of regular cold swimmers in our study. Our research revealed complex relationship between cold exposure, neural signaling, immune response, and thermogenic regulation. One-day cold exposure triggered stress response, including cytokine production in white adipose tissue, subsequently activating brown adipose tissue, and inducing thermogenesis. We further studied systemic immune response, including the proportion of leukocytes and cytokines production. Interestingly, γδ T cells emerged as possible regulators in the broader systemic response, suggesting their possible contribution in the dynamic process of cold adaptation. We employed RNA-seq to gain further insights into the mechanisms by which γδ T cells participate in the response to cold. Additionally, we challenged rats exposed to cold with the Toll-like receptor 2 agonist, showing significant modulation of immune response. These findings significantly contribute to understanding of the physiological acclimation that occur in response to cold exposure.
摘要：
哺乳动物身体对寒冷暴露具有显著的适应性，涉及细胞代谢的复杂调整，最终导致产热。然而,寒冷引起的应激会影响免疫反应，主要通过去甲肾上腺素介导的途径。在我们的研究中,我们利用短期或长期轻度冷暴露的大鼠模型来研究冷适应过程中的全身免疫反应。为了提供人类相关性，我们在研究中纳入了一组常规的冷游泳者。我们的研究揭示了寒冷暴露之间的复杂关系，神经信号，免疫反应，和产热调节。一天的冷暴露引发了应激反应，包括白色脂肪组织中细胞因子的产生，随后激活棕色脂肪组织，并诱导产热。我们进一步研究了全身免疫反应，包括白细胞和细胞因子产生的比例。有趣的是,γδT细胞在更广泛的系统反应中可能作为调节因子出现，表明它们在冷适应的动态过程中可能做出的贡献。我们使用RNA-seq来进一步了解γδT细胞参与冷反应的机制。此外,我们用Toll样受体2激动剂挑战暴露于寒冷的大鼠，显示免疫应答的显著调节。这些发现极大地有助于理解响应于冷暴露而发生的生理适应。
