Objective To investigate the influences of UVA on the secretion and expression of chemokine CXCL11/I-TAC by HaCaT cells induced by interferon γ (IFN-γ) and tumor necrosis factor α (TNF-α). Methods HaCaT cells were cultured in the presence of IFN-7 and TNF-a and irradiated with UVA of 2, 4 and 8 J/cm~2, respectively; those cells receiving neither treatment with IFN-γ or TNF-α nor UVA irradiation served as the negative control, and those receiving only cytokine treatment but no irradiation as the positive control. After another 24-hour culture, enzyme-linked immunosorbent assay (ELISA) was performed to detect the protein levels of CXCL11/I-TAC in the supernatant of HaCaT celb, real time PCR to measure the mRNA expression of CXCL11/I-TAC in these HaCaT cells. Results As far as the negative control HaCaT cells were concerned, there was a minor secretion of CXCL11/I-TAC protein and expression of CXCL11/I-TAC mRNA. After treatment with IFN-7 and TNF-a of 10 μg/L, the protein and mRNA expressions of CXCL11/ I-TAC were synergistically upregulated, whereas the induced secretion and expression of CXCL11/I-TAC by HaCaT cells were dose-dependently inhibited by UVA irradiation. Conclusions UVA irradiation inhibits the secretion and expression of CXCL11/I-TAC by HaCaT cells, which in turn suppresses the chemotaxis of Th1/ Tel cells in some degree.

Objective:To investigate the expression of Th1 chemokine CXCL9,CXCL10,CXCL11,Th2 chemokine CCL22 and their receptors in the lesions of bullous pemphigoid (BP).Methods:Immunohistochemical assay was performed to detect the expression of CXCL9,CXCL10,CXCL11,CCL22 and their receptors CXCR3 and CCR4 in BP lesions and normal control skin.Results:CXCL9,CXCL10,CXCL11,CCL22,CXCR3 and CCR4 were overexpressed in BP lesions than those in normal control skin (P＜0.01).The positive rates of CXCL9,CXCL10,CXCL11 and CXCR3 in BP lesions were 50%(15/30),46.7%(14/30),46.7%(14/30) and 53.3%(16/30),respectively.The positive rates of CCL22 and CCR4 were 66.7% (20/30) and 56.7% (17/30).Conclusion:The overexpression of Th1 chemokine CXCL9,CXCL10,CXCL11,Th2 chemokine CCL22 and their receptors may play important roles in the pathogenesis of BP.