中国人鼻息肉存在Th1/Th2/Th17混合炎症应答的特点，但发病机制不详。抗菌肽LL37可和自身DNA形成复合物促进Th1/Th17极化。而树突状细胞(DCs)是人体最重要的抗原递呈细胞，在鼻息肉发病以及T细胞的极化中起着关键作用。我们前期研究发现LL37在鼻息肉组织中表达增高，鼻息肉中存在LL37-DNA复合物，LL37-DNA体外刺激鼻息肉病人外周血单个核细胞可诱导IFN-γ和IL-17A表达升高，提示LL37-DNA可能促进鼻息肉中Th1/Th17极化，但LL37-DNA调控鼻息肉Th1/Th17极化的机制仍不清。为此，本课题拟通过组织和体外细胞培养系统，探讨LL37-DNA调控外周血来源和鼻息肉组织来源DCs促进鼻息肉Th1/Th17极化的机制和通路。本研究有助于阐明国人鼻息肉中Th1/Th17优势的机制，为探索针对国人鼻息肉发病特点的治疗方法提供思路。

In Chinese, NP shows Th1/Th2/Th17 diversity pattern inflammation. However, the mechanism is unclear. Antimicrobial peptides LL37 was reported to combine with self-DNA and promote Th1/Th17 inflammation. Dendritic cells play a critical role in the pathogenesis of NP and T cells polarization. Recently, our group found that LL37 expression increased in NP and positively correlated with Th1/Th17 inflammation and neutrophil infiltration. And we found LL37-DNA complex in nasal polyps tissue. Moreover, we used LL37-DNA complex to stimulate peripheral blood monocytes (PBMCs) from NP and found elevation of IFN-γ and IL-17A in supernatant. However, the mechanism is unclear. Thus, we hypothesize that LL37-DNA overexpression in NP could modulate DCs and promote T-helper cells polarization. To address this issue, we plan to separate PBMCs-DCs and NP-DCs and stimulate with LL37-DNA, and co-culture naïve CD4+ T cells from PBMCs, then analyze the immunomodulatory effect of LL37-DNA on Th1/Th17 inflammation and the mechanism. This study may elucidate an important molecular mechanism underlying the pathogenesis and potential treatment target of NP.