摘要
介紹：類風濕性關節炎是自體免疫疾病，受到遺傳因子及環境因素的影響。F11R與發炎細胞移動有關，也是芳香烴受體的目標基因，而芳香烴受體受到很多環境因子的作用。F11R可能是連接環境因素與類風濕性關節炎一個橋樑。 目的:我們想了解： (1)F11R在類風濕性關節炎病人表現是否確實增加？(2)F11R是否與類風濕性關節炎某些症狀或徵象相關？(3) F11R與發炎指標關係為何？ 材料與方法: 從類風濕性關節炎病人及正常人中，抽取周邊血液單核球中核糖核酸及周邊血液去氧核醣核酸。利用即時定量聚合酶連鎖反應偵測F11R之mRNA表現量。以SNP genotyping assay進行基因多型性鑑定。以酵素連結免疫分析法測定血漿中IFN-γ表現量。 結果: F11R 在類風濕性關節炎患者的周邊血液單核球表現量比普通人多（p =0.018）。患者有唾腺侵犯時，F11R數值較低 (p= 0.037)。但F11R與其他次發性乾燥症症狀相關性不顯著。F11R啟動子-688 A＞C，C carrier有較低的anti-CCP (p=0.002) 及較少的淚腺問題(p=0.009)。校正DR4的干擾後，這現象依然存在。在類風濕關節炎病人，F11R啟動子-688 A＞C 和 -436 A>G兩個位置基因多型性與基因表現量不相關。IFN-γ在類風濕性關節炎病人的表現量和F11R並沒有顯著相關。 討論：F11R在類風濕性關節炎的病人表現量較高，與幫助發炎細胞通過細胞間隙的功能有關。F11R病人唾腺功能不良時數值較低，可能與它在此族群細胞間隙表現量減少有關。F11R啟動子 -688 A變異為C時，對病人有保護作用。IFN-γ在類風濕性關節炎病人與F11R作用，需要進一步實驗才能釐清。
並列摘要
Introduction: Rheumatoid arthritis is an autoimmune disease, which is affected by genetic and environmental factors. F11R is associated with inflammatory cells migration and also the target gene of aryl hydrocarbon receptor. The aryl hydrocarbon receptor is triggered by multiple environmental factors. F11R may link environmental factors to rheumatoid arthritis. Aim: We investigate whether (1) F11R expression increases in rheumatoid arthritis? （2）F11R is associated with rheumatoid arthritis characteristics ? and（3）F11R is associated with inflammatory markers? Material and Methods: We extracted RNA from peripheral blood mononuclear cells and DNA from peripheral blood in rheumatoid arthritis patients and control group. F11R mRNA expression was determined by real time PCR. SNP genotyping assay was done for single nucleotide polymorphism. IFN-γ was quantified by enzyme-link immunosorbent assay. Results: F11R expression in peripheral blood mononuclear cells is more in rheumatoid arthritis patients than control group (p = 0.018). F11R expression is lower in patients who has impaired salivary gland function than control group (p= 0.037). F11R association with other secondary Sjögren’s syndrome characteristics is not significant. In F11R promoter -688 A＞C, C carrier possesses lower anti-CCP（p=0.002）and lacrimal gland problems(p=0.009). Both are significant after correcting DR4 existence. Different SNP genotype in F11R promoter -688 A＞C and -436 A>G doesn’t lead to different gene expression in rheumatoid arthritis patients. IFN-r amount in rheumatoid arthritis is not correlated with F11R. Discussion: F11R’s role in inflammatory cell migration explains its higher expression in rheumatoid arthritis patients. The lower F11R expression in subgroup with impaired salivary gland function may be related with less intercellular junction expression. C carrier in F11R promoter -688 A＞C locus seems protective. The relation of IFN-γ and F11R in rheumatoid arthritis patients needs more studies to clarify.