Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021
Cross-talk between CXC chemokine ligand 10-CXC chemokine receptor 3 axis and CC chemokine ligand 17-CC chemokine receptor 4 axis in the pathogenesis of oral lichen planus.
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Tang Nan, Zhang Yu-Yao, Cheng Jue-Hua, Zhao Zhi-Bai, Fan Yuan
Аннотация
OBJECTIVES: This study aimed to determine whether a correlation existed between CXC chemokine ligand 10 (CXCL10)-CXC chemokine receptor 3 (CXCR3) and CC chemokine ligand 17 (CCL17)-CC chemokine receptor 4 (CCR4) in the pathogenesis of oral lichen planus (OLP).
METHODS: Peripheral blood of OLP patients (non-erosive and erosive groups) and healthy controls were collected, and T cells were isolated and purified. T cells were co-cultured with three groups: blank, anti-CXCR3, and anti-CCR4. CXCR3 and CCR4 expression were detected by flow cytometry, and CXCL10 and CCL17 were detected by enzyme-linked immunosorbent assay, respectively.
RESULTS: The purities of T cells were all >95% in the three groups (P>0.05). Receptor expression showed that CXCR3 and CCR4 in the anti-CXCR3 group was downregulated in OLP compared with the blank group (P>0.05). The level of CCR4 in the anti-CCR4 group was significantly downregulated (P<0.05), and CXCR3 was upregulated (P>0.05). Ligand analysis results showed that CXCL10 in the anti-CXCR3 group was significantly downregulated in OLP compared with the blank group (P<0.05), and CCL17 was also downregulated (P>0.05). CCL17 in the anti-CCR4 group was significantly downregulated (P<0.05), and CXCL10 was upregulated (P>0.05). The trend of receptors and ligands in controls was consistent with OLP, but no significant difference existed between the antagonistic and the blank groups (P>0.05).
CONCLUSIONS: Two axes interact with each other in the pathogenesis of OLP and may play different roles in its occurrence and development.
METHODS: Peripheral blood of OLP patients (non-erosive and erosive groups) and healthy controls were collected, and T cells were isolated and purified. T cells were co-cultured with three groups: blank, anti-CXCR3, and anti-CCR4. CXCR3 and CCR4 expression were detected by flow cytometry, and CXCL10 and CCL17 were detected by enzyme-linked immunosorbent assay, respectively.
RESULTS: The purities of T cells were all >95% in the three groups (P>0.05). Receptor expression showed that CXCR3 and CCR4 in the anti-CXCR3 group was downregulated in OLP compared with the blank group (P>0.05). The level of CCR4 in the anti-CCR4 group was significantly downregulated (P<0.05), and CXCR3 was upregulated (P>0.05). Ligand analysis results showed that CXCL10 in the anti-CXCR3 group was significantly downregulated in OLP compared with the blank group (P<0.05), and CCL17 was also downregulated (P>0.05). CCL17 in the anti-CCR4 group was significantly downregulated (P<0.05), and CXCL10 was upregulated (P>0.05). The trend of receptors and ligands in controls was consistent with OLP, but no significant difference existed between the antagonistic and the blank groups (P>0.05).
CONCLUSIONS: Two axes interact with each other in the pathogenesis of OLP and may play different roles in its occurrence and development.