Tang Yi, Zhu Xiaoxia, Han Rui, Zhou Qiang, Cheng Hao
Department of Dermatology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou.
Department of Dermatology, Ningbo First Hospital, Ningbo, Zhejiang.
Medicine (Baltimore). 2020 Feb;99(8):e19214. doi: 10.1097/MD.0000000000019214.
Langerhans cells (LCs) and plasmacytoid dendritic cells (pDCs) play an important role in the cutaneous immune response to viral infection. Verruca vulgaris (VV) is a chronic benign disease caused by human papillomavirus (HPV) infection.To investigate the possible roles of LCs, pDCs and toll-like receptor (TLR)7/9 signaling pathways in the pathogenesis of VV, we detected the expression of CD1a, CD2AP, CD123, TLR7/9, IFN regulatory factor 7 (IRF7), and interleukin-1 receptor-associated kinase 1 (IRAK1) in VV lesions.The expression of CD1a, CD2AP, CD123, TLR7/9, IRF7, and IRAK1 in 20 VV lesions was tested by immunohistochemistry. The density and number of stained cells were compared between VV lesions and the perilesional normal skin.The density and number of CD1a-, CD2AP-, CD123-, TLR9-, and IRAK1-positive cells in the papillary layer of VV lesions were significantly higher than those in the perilesional normal skin (P < .05). There were no significant differences in the density and positive rate of CD1a+ cells in the epidermis and of TLR7 and IRF7 cells in the dermis between VV lesions and the perilesional normal skin at the edge (P > .05).In VV, the number of LCs increases only in the dermis, indicating that LC's antigen-presenting function might not be inhibited. The increased number of pDCs in VV lesions suggests that HPV infection may recruit the pDCs to the virus-infected epithelium. We speculate that the TLR7/9 downstream signaling pathway is not fully activated in VV, leading to difficulty of HPV removal and the relapse of HPV-infected lesions.
朗格汉斯细胞（LCs）和浆细胞样树突状细胞（pDCs）在皮肤对病毒感染的免疫反应中起重要作用。寻常疣（VV）是由人乳头瘤病毒（HPV）感染引起的慢性良性疾病。为了研究LCs、pDCs和Toll样受体（TLR）7/9信号通路在VV发病机制中的可能作用，我们检测了VV病变中CD1a、CD2AP、CD123、TLR7/9、干扰素调节因子7（IRF7）和白细胞介素-1受体相关激酶1（IRAK1）的表达。通过免疫组织化学检测20例VV病变中CD1a、CD2AP、CD123、TLR7/9、IRF7和IRAK1的表达。比较VV病变与病变周围正常皮肤中染色细胞的密度和数量。VV病变乳头层中CD1a、CD2AP、CD123、TLR9和IRAK1阳性细胞的密度和数量显著高于病变周围正常皮肤（P<0.05）。VV病变与边缘病变周围正常皮肤之间，表皮中CD1a+细胞的密度和阳性率以及真皮中TLR7和IRF7细胞的密度和阳性率均无显著差异（P>0.05）。在VV中，LCs数量仅在真皮中增加，表明LCs的抗原呈递功能可能未被抑制。VV病变中pDCs数量增加表明HPV感染可能将pDCs招募到病毒感染的上皮细胞。我们推测，TLR7/9下游信号通路在VV中未被完全激活，导致HPV难以清除且HPV感染病变复发。
