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该研究发现，长链非编码RNA——Lnc-Atg16l1的茎环结构变化促进小鼠TLR-MyD88依赖性炎症和自身免疫反应。 研究证明Lnc-Atg16l1可以结合活化的TLR7，通过促进TLR7与MyD88的相互作用，增强TLR7信号通路和炎症。 还证明了LncAtg16l1的茎环结构变化在促进TLR7信号传导中起重要作用，这在小鼠SLE模型中也得到了证实。 该研究报道了内源LncRNA Lnc-Atg16l1增强TLR7-MyD88免疫信号通路和促进自身免疫病发生的功能，并为其调控机制提出了新见解 。
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该研究表明Lnc-Atg16l1的茎环改变促进小鼠TLR7-MyD88依赖性炎症和自身免疫。 该研究通过iCLIP-seq鉴定了TLR7结合的长链非编码RNA Lnc-Atg16l1，并发现它在各种类型的免疫细胞中促进TLR7和其他MyD88依赖的TLR信号传导。 Yang z, ji s, liu l, liu s, wang b, ma y, cao x 该研究发现，长链非编码RNA—— Lnc-Atg16l1 的茎环结构变化促进小鼠TLR-MyD88依赖性炎症和自身免疫反应。 这一发现为自体RNA的促炎功能提供了结构依赖性的见解，并为与TLR相关的自身免疫疾病 （例如系统性红斑狼疮） 提供了潜在的治疗靶点。
