SLE是近年來最常被研究會侵犯多重器官系統的自體免疫疾病（Autoimmune Disease）。其廣泛的牽涉了II~IV型的過敏反應，過敏反應的過分激活為自體抗體大量產生引發細胞apoptosis的潛在因素，在本實驗室過去曾發現在NZB/W F1 mice作為實驗動物模式之下，以cystamine此TG2及caspase的抑制劑具有在血清學及蛋白檢測中均可透過抑制細胞的凋亡，進而減緩SLE達到保護的作用，改善狼瘡病症，且延長其存活率。為了同時在免疫方面觀察胱胺是否也有著能減緩SLE的傾向，進而深入了解觀察腎臟這個重要的次級免疫器官，探討cystamine是否對於腎臟也具有重要的調節作用進而能改善病症，在本實驗中以flow cytometry對免疫傾向的確認，透過CD8/CD4/CD25 maker觀察TH1/TH2 balance，發現胱胺能有效的反轉SLE大量傾向TH2進而產生的自體抗體，同時也能增加 Treg的高量表達進而去抑制免疫反應緩解發炎。另外，透過了反轉錄聚合鏈鎖反應(reverse transcription-polymerase chain reaction, RT-PCR)觀察spleen中CD8/CD4 maker的mRNA表現量比較TH1/TH2 balance的傾向，發現經過胱胺處理後的確TH1相關的CD8 maker的mRNA比例量有大幅度上升，間接證明SLE傾向於TH2有被反轉，而在Treg的特異性 maker方面CD25/ Foxp3之mRNA之比例也有大量上升，T cell的活性化maker CD40L也減少了mRNA的表現量，同時證實了SLE免疫傾向的反轉，及發炎情況的減少及Treg cell的大量誘發。在處理了kidney石臘切片後，染以PAS、tricrome stain觀察基底膜及以HE stain觀察細胞形態、IHC觀察免疫複合物沉積，發現在第26週大未處理胱胺的NZB/W F1切片中便可觀察到免疫複合物沉積，經過14天的胱胺處理後相對於未處理胱胺出現臨床病徵上70% SLE均會產生的SLE活性化之腎病變之情況有減少的傾向，同時觀察狼瘡病徵中被發現因自由基的過度產生脂質過氧化情況及使得抗自由基分子(GSH、catalase等等)的減少現象在經過胱胺處理後也大幅度的趨向正常，由以上的各個結果均佐證胱胺的確能緩解SLE。
In recent years, Systemic Lupus Erythematosus (SLE) can encroach upon many organs in various organs. SLE is involved in immediate allergic II~IV types reactions. The overexpression of immediate allergic reactions can be the potential factor to induce cell apoptosis. In the past researches, cystamine which is the inhibitor of TG2 and caspase can slow down the expression of SLE through suppressing cell apoptosis and also can prolong the ratio of surviving in NZB/W F1 mice model in serological and protein test. We use the kidney to research the issue of that cystamine can regulate kidney to improve the disease or not. In flow cytometry, we use CD8/CD4/CD25 makers to observe the balance of TH1/TH2, and we find that cystamine can raise TH2 expression to produce autoantibodies and also can induce overexpression of Treg to ease inflammation. In othor way, we use RT-PCR to observe the secretion of mRNA to compare with the balance of TH1/TH2 in spleen, so that we can see if we treat with cystamine can apparently raise the ratio of TH1 and also raise mRNA of CD25/ Foxp3, but reduce mRNA of CD40L. As a result of kidney which is the important secondary immunity organ discusses cystamin whether is the important control action or not to regulate in kidney then to be able to improve illness. Once showed in the past literature that the Treg cell acts a very important role in regarding the immunity tolerance. We can find in this experiment that cystamin may activate the Treg suppression in NZB/W F1 mice from the autoantibodies response and perhaps it will have to be allowed to become the treatment SLE the auxiliary medicine and healthy food hopes.
