The full array of cold-responsive cell types within white adipose tissue that drive thermogenic beige adipocyte biogenesis remains undefined. We demonstrate that acute cold challenge elicits striking transcriptomic changes specifically within DPP4+ PDGFRβ+ adipocyte precursor cells, including a β-adrenergic receptor CREB-mediated induction in the expression of the prothermogenic cytokine, Il33. Doxycycline-inducible deletion of Il33 in PDGFRβ+ cells at the onset of cold exposure attenuates ILC2 accumulation and beige adipocyte accrual. These studies highlight the multifaceted roles for adipocyte progenitors and the ability of select mesenchymal subpopulations to relay neuronal signals to tissue-resident immune cells in order to regulate tissue plasticity.

中文翻译：

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冷反应性脂肪细胞祖细胞将肾上腺素能信号传导与免疫细胞激活相结合，以促进米色脂肪细胞的生长

白色脂肪组织内驱动产热米色脂肪细胞生物发生的全部冷反应细胞类型仍未确定。我们证明，急性寒冷挑战会在 DPP4+ PDGFRβ+ 脂肪细胞前体细胞内引起显着的转录组变化，包括 β-肾上腺素能受体 CREB ​​介导的促生细胞因子Il33表达的诱导。在冷暴露开始时，PDGFRβ+ 细胞中多西环素诱导的 Il33 缺失减弱了 ILC2 的积累和米色脂肪细胞的积累。这些研究强调了脂肪细胞祖细胞的多方面作用以及选择间充质亚群将神经元信号传递给组织驻留免疫细胞以调节组织可塑性的能力。