Type 2 innate lymphoid cells constitutively express arginase-I in the naive and inflamed lung
Type 2 innate lymphoid cells constitutively express arginase-I in the naive and inflamed lung
复制标题
DOI：
10.1189/jlb.0213084
复制
发表时间：
2013-11-01
影响因子：
5.5
通讯作者：
Locksley, Richard M.
中科院分区：
文献类型：
--
作者：
Bando, Jennifer K.;Nussbaum, Jesse C.;Locksley, Richard M.
Arg1是由AAM产生的，被认为在哮喘和过敏性炎症过程中具有调节作用。在这里，我们使用Arg1报告小鼠来确定肺中该酶的其他细胞来源。我们证明了ILC2s在静息和感染迁徙蠕虫巴西尼波斯壮线虫期间表达Arg1。与AAM不同的是，AAM在IL-4/IL-13介导的STAT6激活后表达Arg1，而ILC2以STAT6不依赖的方式结构性地表达该酶。尽管IL-33R亚单位T1/ST2缺陷的ILC2维持Arg1的表达，但IL-33可以通过扩大ILC2群体和通过STAT6间接激活巨噬细胞来调节总肺Arg1。最后，我们发现ILC2 Arg1并不介导ILC2的积聚，ILC2产生IL-5和IL-13，或在新月形虫感染过程中产生胶原。因此，ILC2是静息组织和过敏性炎症期间Arg1的新来源。
Arg1 is produced by AAMs and is proposed to have a regulatory role during asthma and allergic inflammation. Here, we use an Arg1 reporter mouse to identify additional cellular sources of the enzyme in the lung. We demonstrate that ILC2s express Arg1 at rest and during infection with the migratory helminth Nippostrongylus brasiliensis. In contrast to AAMs, which express Arg1 following IL-4/IL-13-mediated STAT6 activation, ILC2s constitutively express the enzyme in a STAT6-independent manner. Although ILC2s deficient in the IL-33R subunit T1/ST2 maintain Arg1 expression, IL-33 can regulate total lung Arg1 by expanding the ILC2 population and by activating macrophages indirectly via STAT6. Finally, we find that ILC2 Arg1 does not mediate ILC2 accumulation, ILC2 production of IL-5 and IL-13, or collagen production during N. brasiliensis infection. Thus, ILC2s are a novel source of Arg1 in resting tissue and during allergic inflammation.