Expressionof langerhans cell and plasmacytoid dendritic cell markers, and toll-like receptor 7/9 signaling pathway proteins in verruca vulgaris lesions

被引:9
|
作者
Tang Yi [1 ]
Zhu Xiaoxia [2 ]
Han Rui [3 ]
Zhou Qiang [3 ]
Cheng Hao [3 ]
机构
[1] Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Dermatol, Hangzhou, Peoples R China
[2] Ningbo First Hosp, Dept Dermatol, Ningbo, Zhejiang, Peoples R China
[3] Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Dermatol, Qingchun East Rd 3, Hangzhou, Peoples R China
关键词
langerhans cell; plasmacytoid dendritic cell; toll-like receptor; verruca vulgaris; I INTERFERON; INFECTION; RESPONSES;
D O I
10.1097/MD.0000000000019214
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
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页数:8
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