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DC-SIGN(DC-specificICAM-grabbingnon-integrin,亦称CD209)属树突状细胞(DC)表面C型凝集素的膜蛋白。作为DC黏附及模式识别受体,其参与介导了DC的炎症组织迁移,识别捕获病原微生物,以及随后激活静息T细胞启动的免疫应答。为此观察了DC-SIGN及DC-SIGN+DC在肾炎患者肾组织中表达和分布,以及DC-SIGN在炎性状态下培养人肾小管上皮细胞表达,探讨与肾小管间质炎症病变和损伤的关系。结果显示,DC-SIGN在正常肾组织基本不表达,而在肾炎早期即以肾小管上皮细胞为主表达上调,且随肾小管间质病变程度加重表达增强(P<0.01),与肾小管间质病变程度明显相关(P<0.01)。此外,DC-SIGN在经TNF-α刺激炎性状态下的人肾小管上皮细胞也明显表达。进一步发现,DC-SIGN+DC在肾炎早期以肾间质为主分布聚集,也随肾小管间质病变程度加重明显增多(P<0.01),与肾小管间质病变程度显著相关(P<0.01),也与DC-SIGN表达相关联(P<0.01)。另外,DC-SIGN+DC在肾小管间质分布数量与肾炎患者肾功能改变明显相关(P<0.05)。研究结果提示,DC-SIGN也是肾小管间质早期炎症的启动参与因素,其介导DC可能也参与了人肾炎肾小管间质的免疫损伤机制。
DC-SIGN (DC-specific ICAM-grabbing non-integrin, also known as CD209) is a membrane protein of C-type lectin on the surface of dendritic cells. As a DC adhesion and pattern recognition receptor, it is involved in mediating the migration of inflammatory tissues of DCs, recognizing the capture of pathogenic microorganisms, and subsequent activation of resting T cell-initiated immune responses. Therefore, we observed the expression and distribution of DC-SIGN and DC-SIGN + DC in renal tissue of nephritis patients and the expression of DC-SIGN in human renal tubular epithelial cells in inflammatory state, Relationship. The results showed that DC-SIGN was not expressed in normal renal tissues, but mainly in renal tubular epithelial cells in the early phase of nephritis, which was up-regulated with the degree of tubulointerstitial lesions (P <0.01) Quality of disease was significantly correlated (P <0.01). In addition, DC-SIGN is also significantly expressed in human renal tubular epithelial cells that are TNF-α-stimulated inflammatory. It was further found that DC-SIGN + DC accumulated mainly in the early stages of glomerulonephritis with interstitial interstitial fibrosis, but also with the severity of tubulointerstitial lesions (P <0.01), and significantly correlated with the degree of tubulointerstitial lesions (P <0.01 ), Also associated with DC-SIGN expression (P <0.01). In addition, the number of DC-SIGN + DC in the tubulointerstitial was significantly correlated with renal function in patients with nephritis (P <0.05). The results suggest that DC-SIGN is also involved in the initiation of early tubulointerstitial inflammation, and its mediation of DC may also be involved in the renal tubular interstitial immune injury mechanism.