• 作者： 余家利; 蔡長祐; 曲敬正; 廖堂順; 林虎美; 姜必寧; 韓韶華; 王世叡
• 作者服務機構： 台北榮民總醫院過敏免疫風濕科; 國立陽明醫學院臨床醫學研究所; 國立陽明醫學院微生物暨免疫研究所
• 中文摘要： 在我們先前的報告中發現全身性紅斑狼瘡病人的吞食細胞及淋巴細胞的機能有異常。為了進一步了解這些免疫關聯細胞機能異常的原因，我們研究了25位活動期全身性紅斑狼瘡病人，10位長期服用類固醇的支氣管氣喘病人，以及25位年齡、性別相仿的健常人白血球膜上C3b接受體的表現、A23187刺激之後 Ca的攝取、粒腺體的電位差以及吞食機能。我們發現狼瘡病人白血球的自發性（為健常人的37.2±3.7％）及經FMLP刺激之後（為健常人的68.3±7.1％）膜上C3b接受體的表現降低。但是長期接受類固醇治療的氣喘病人白血球上C3b接受體的表現與健常人相同。而且狼瘡病人白血球的粒腺體活性及經A23187刺激之後Ca-influx幾乎正常。這個結果顯示狼瘡病人白血球吞食機能的缺陷乃存在於認知期而非吞噬期。在另一方面，狼瘡病人的淋巴球對於PHA刺激反應低下（病人淋巴球的刺激指數為127.4±46.3，健常人的刺激指數為311.2±30.4，兩者之間有明顯的差異（P=0.0077）。因此，我們進一步測定個別細胞的膜電位差。發現病人淋巴球在沒有刺激之下呈現高電位，但是經PHA刺激三天之後，其膜電位差反而比正常淋巴球為低，病人淋巴球的NaK-ATPase的活性亦呈同一傾向。長期服用類固醇氣喘病人淋巴球的膜電位差及NaK-ATPase的變化幾與健常人無異。綜合這些結果，我們的結論是狼瘡病人白血球膜上C3b接受體的減少，以及淋巴球產生NaK-ATPase的能力不足導至病人細胞性防禦機能有缺陷，而易受感染。
• 英文摘要： In our previous report, we demonstrated that the functions of phagocytes and lymphocytes weredefective in patients with systemic lupus erythematosus (SLE). In an attempt to further clarify the defectivemechanisms of these cells, 25 active SLE, 10 bronchial asthma patients (BA) on corticosteroids and 25 age andsex-matched normal individuals were investigated for the expression of membraneous C3b receptors,ionophore-induced -uptake, mitochondrial potentials and phagocytic activity of neutrophils. Wefound decreased expression of C3b receptors on SLE PMN in both resting (37.2 ± 3.7% of the normalcontrols) and FMLP-stimulated (68.3 ± 7.1% of the normal controls) conditions, whereas the C3breceptor expression on BA-PMN receiving long-term steroid treatment was not different from normal controls.This suggests that the defective phagocytosis of SLE PMN is in the recognition, but not in the ingestion phasebecause of the normal function of -influx and mitochondrial activity in SLE PMN. On the other hand,hyporesponsiveness to PHA stimulation (stimulation index: 127.4 ± 46.3 in SLE vs. 311.2 ± 30.4 in normals,p=0.0077) was a distinct cell-mediated immune abnormality in our SLE patients. We measured themembrane potential of individual cells using 3,3′ -dihexyloxacarbocyanin and found hyperpolarization inresting SLE lymphocytes. However, the membrane polarization of SLE lymphocytes became lower than thatof normal cells after PHA stimulation for 3 days A similar tendency was also found in -dependentATPase activity in SLE lymphocytes. Putting these together, we conclude that decreased C3b receptorexpression on neutrophils and defective generation of -ATPase in lymphocytes are responsible for theimpaired cellular defense mechanisms in patients with SLE.
• 中文關鍵字： phogocytosis; C3b receptor; membrane potential; NaK-ATPase.
• 英文關鍵字： --