Fas抗原(CD95),是屬於腫瘤壞死因子及神經生長因子族群中之一橫跨細胞膜之蛋白,其功能主要為釋放細胞“凋零”之訊息于其標的細胞。本研究,我們使用流體細胞儀及單株抗體(Anti-Fas)去測試僵直性脊椎炎與其它自體免疫病-類風濕關節炎(RA)與全身性紅斑性狼瘡(SLE)其周邊血單核細胞之Fas與CD45RO抗原。其結果顯示在全血與無PHA刺激下,紅斑性狼瘡病人血中單核球之Fas抗原較正常人顯著增加。而類風濕、關節炎及僵直性脊椎炎(AS)等風濕病患者之血中單核細胞Fas抗原與正常人比較,無明顯差異。而CD45RO(記憶細胞)在上述不同疾病之患者與正常人比較皆無明顯增加。在PHA刺激下,不論類風溼性關節炎、紅斑性狼瘡與僵直性脊椎炎患者及正常人,刺激2日後,其單核球Fas抗原皆較無刺激時明顯增加。然而CD45RO在紅斑性狼瘡與僵直性脊椎炎患者較正常人明顯地增加。另一亦可活化淋巴球刺激物TNF-α其作用不論對Fas或CD45RO表現皆較PHA有明顯之差別。另外Fas抗原表現與CD45RO表現並未成正相關。總結,不同風濕免疫病其經由FAS抗原導致細胞凋零之機轉不盡相同。僵直性脊椎炎,為一發炎性脊椎之疾病,在患者周邊血中單核球並未明顯表現Fas及CD45RO抗原。進一步研究有關其周邊關節炎滑膜細胞是否有凋零類似類風濕關節炎,可暸解此病變之可能致病機轉。
Fas antigen (CD95), a transmembrane protein of the tumor necrosis factor and nerve growth factor family, is a well known mediator of apoptosis, which transfer apoptotic signal into the target cells. In this study, we measured Fas and CD45RO antigens on peripheral blood mononuclear cells (PBMC) in ankylosing spondylitis (AS) and compared simultaneously with autoimmune diseases, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), by using flow cytometric analysis. The results showed a significant increase of Fas antigen on PBMC (without mitogen stimulation) in patients with SLE when compared with the normal control. There was no significant difference, however, in RA and AS. With PHA stimulation, including RA, SLE, AS and normal control, Fas on PBMC increased significantly after 2 days of in vitro culture. However, for CD45RO antigen (memory cells), there was a significant increase only in patients with AS and SLE. TNF-����, one of the mitogens for lymphocytes activation, did not work as well as PHA to stimulate Fas or CD45RO antigen expression. The presence of Fas is not correlated with CD45RO antigen in this study. In summary, the Fas-mediated apoptosis as an immunopathogenesis in different rheumatic or immune diseases may be variable. AS, an inflammatory spinal disease, did not show a significant increase in Fas and CD45RO����antigens in PBMCs. Further study on synovial membrane mononuclear cells may provide a better understanding whether Fas-mediated apoptosis, like RA, will develop in this HLA-B27-related disease.