The JmjC protein Mina is an important immune response regulator. Classical forward genetics first discovered its immune role in 2009 in connection with the development of T helper 2 (Th2) cells. This prompted investigation into Mina's role in the two best-studied contexts where Th2 responses are essential: atopic asthma and helminth expulsion. In work focused on a mouse model of atopic asthma, Mina deficiency was found to ameliorate airway hyper-resistance and pulmonary inflammation. And, in a case-control study genetic variation at the human MINA locus was found to be associated with the development of childhood atopic asthma. Although the underlying cellular and molecular mechanism of Mina's involvement in pulmonary inflammation remains unknown, our recent work on parasitic helminth expulsion suggests the possibility that, rather than T cells, epithelial cells responding to TGFβ may play the dominant role. Here we review the growing body of literature on the emerging Mina pathway in T cells and epithelial cells and attempt to set these into a broader context.

中文翻译：

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Mina：Th2 反应调节器满足 TGFβ。

JmjC 蛋白 Mina 是一种重要的免疫反应调节剂。经典正向遗传学于 2009 年首次发现其与 T 辅助 2 (Th2) 细胞发育相关的免疫作用。这促使对 Mina 在 Th2 反应必不可少的两个研究最充分的情况下的作用进行调查：特应性哮喘和蠕虫排出。在专注于特应性哮喘小鼠模型的工作中，发现 Mina 缺乏可改善气道高阻和肺部炎症。而且，在一项病例对照研究中，发现人类 MINA 基因座的遗传变异与儿童特应性哮喘的发展有关。尽管 Mina 参与肺部炎症的潜在细胞和分子机制仍然未知，但我们最近在寄生虫驱除方面的工作表明，有可能，对 TGFβ 有反应的上皮细胞可能起主导作用，而不是 T 细胞。在这里，我们回顾了越来越多的关于 T 细胞和上皮细胞中出现的 Mina 通路的文献，并试图将它们置于更广泛的背景中。