Influence of the transcription factor RORγt on the development of NKp46+ cell populations in gut and skin
Influence of the transcription factor RORγt on the development of NKp46+ cell populations in gut and skin
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DOI：
10.1038/ni.1681
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发表时间：
2009-01-01
影响因子：
30.5
通讯作者：
Tomasello, Elena
中科院分区：
文献类型：
--
作者：
Luci, Carmelo;Reynders, Ana;Tomasello, Elena
从血液、淋巴器官、肺、肝和子宫中分离的NKp 46（+）CD 3（-）自然杀伤淋巴细胞可产生颗粒依赖性细胞毒性和干扰素-γ。在这里，我们确定在真皮，肠固有层和cryptopatches不同群体的NKp 46（+）CD 3（-）细胞的能力减弱，去角质和产生干扰素-γ。在肠道中，参与淋巴组织诱导细胞发育的转录因子ROR γ t的表达定义了以前未知的NKp 46 + CD 3-淋巴细胞亚群。与ROR γ t（-）固有层和真皮自然杀伤细胞不同，肠道ROR γ t（+）NKp 46（+）细胞产生白细胞介素22。我们的数据显示，淋巴组织诱导细胞和自然杀伤细胞具有意想不到的相似性，并强调了NKp 46（+）CD 3（-）细胞在先天免疫，淋巴组织和局部组织修复中的异质性。
NKp46(+)CD3(-) natural killer lymphocytes isolated from blood, lymphoid organs, lung, liver and uterus can produce granule-dependent cytotoxicity and interferon-gamma. Here we identify in dermis, gut lamina propria and cryptopatches distinct populations of NKp46(+)CD3(-) cells with a diminished capacity to degranulate and produce interferon-gamma. In the gut, expression of the transcription factor ROR gamma t, which is involved in the development of lymphoid tissue-inducer cells, defined a previously unknown subset of NKp46+CD3- lymphocytes. Unlike ROR gamma t(-) lamina propria and dermis natural killer cells, gut ROR gamma t(+)NKp46(+) cells produced interleukin 22. Our data show that lymphoid tissue-inducer cells and natural killer cells shared unanticipated similarities and emphasize the heterogeneity of NKp46(+)CD3(-) cells in innate immunity, lymphoid organization and local tissue repair.