RORgammat and commensal microflora are required for the differentiation of mucosal interleukin 22-producing NKp46+ cells.
RORgammat and commensal microflora are required for the differentiation of mucosal interleukin 22-producing NKp46+ cells.
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肠道的粘膜免疫系统被一层上皮细胞与大量的微生物分开。来自共生菌群的信号是维持上皮稳态所必需的，但这些信号的分子和细胞特性尚不清楚。在这里，我们提供的证据表明，来自共生菌群的信号有助于淋巴细胞群的分化，这些淋巴细胞群共同表达刺激性自然杀伤细胞受体和产生白细胞介素22 （IL-22）的转录因子RORγt。这些产生il -22的RORγthiNKp46+NK1.1int细胞的出现依赖于RORγt的表达，这表明这些细胞可能来源于淋巴组织诱导细胞。这些细胞释放的IL-22促进了在维持粘膜稳态中重要的抗菌分子的产生。
The mucosal immune system of the intestine is separated from a vast array of microbes by a single layer of epithelial cells. Cues from the commensal microflora are needed to maintain epithelial homeostasis, but the molecular and cellular identities of these cues are unclear. Here we provide evidence that signals from the commensal microflora contribute to the differentiation of a lymphocyte population coexpressing stimulatory natural killer cell receptors and the transcription factor RORγt that produced interleukin 22 (IL-22). The emergence of these IL-22-producing RORγthiNKp46+NK1.1int cells depended on RORγt expression, which indicated that these cells may have been derived from lymphoid tissue–inducer cells. IL-22 released by these cells promoted the production of antimicrobial molecules important in the maintenance of mucosal homeostasis.