實驗室過去證實血生性癌細胞能與肺臟血管內皮細胞上CD26 (dipeptidyl peptidase IV)結合，而促進癌細胞轉移。除了肺臟的血管內皮細胞之外，CD26也會表達在免疫細胞的表面上。文獻指出CD26在免疫細胞對抗感染病症上扮演負調控角色。臨床統計資料亦明確顯示，癌症病患體內免疫細胞CD26高表達者其預後情況(prognosis)較差。先前本實驗室已發現轉移癌細胞在經由血液循環轉移的過程中，會誘發小鼠體內先天免疫細胞(innate immune cells)表面上CD26表達的增高，因而抑制其細胞毒殺之能力。同時，亦已發現轉移癌細胞在體外(ex vivo)環境中，無法誘發先天免疫細胞表面CD26表達的升高，這表示尚有其它體內的因子參與此CD26誘發反應。文獻指出轉移癌細胞可召集骨髓衍生抑制細胞(myeloid-derived suppressor cells, MDSC)至血液循環中抑制免疫細胞的功能，但實驗發現小鼠骨髓衍生抑制細胞並未參與此抑制機制。在體內血液循環中，血管內皮細胞與全血血球細胞是體外環境中沒有的因子，經實驗證實血管內皮細胞參與轉移癌細胞誘發先天免疫細胞表面CD26高表達，進而抑制其毒殺能力，而全血血球細胞則不參與。我們更進一步地在體外實驗發現，經轉移癌細胞刺激之血管內皮細胞，其所分泌的條件培養液(conditioned media)即足以誘發先天免疫細胞表面CD26高表達並抑制其毒殺能力。文獻指出，先天免疫細胞功能的活化或抑制會受不同的細胞激素(cytokine)和趨化因子(chemokine)所調控。我們亦利用高通量微珠式蛋白偵測技術(Flowcytomix)偵測到受癌細胞刺激之內皮細胞所分泌的條件培養液中，介白素第六因子(IL-6)的表達量增加。

　In our previous data, we demonstratedthat metastatic cancer cells binded to CD26, which is an adhesison molecule on lung endothelail cells. CD26 not only expressed in lung endothelial cells but also in immune cells. CD26 overexpressed in immune cells plays a role of negative regulating in host immunity against microbes.In clinical investigation,CD26 overexpressed in immune cellsof cancer patients consider revising bad prognosis.In our previous data, we demostrated metastastic tumor cell-induced CD26 upregulation in innate immune cells resulting in cytotoxic suppression.Ex vivo, we demostrated metastatic cancer cells can’t directly induce CD26 overexpress in immune cells.This data suggesting us that another factors to participate in the inhibited mechanism. Metastatic cancer cells recruitedmyeloid-derived suppressor cellsto bloodstream resulte in suppression of immune cells. But in our experiment,CD26 upregulation of innate immune cells can’t be induce by metastatic cancer cells via myeloid-derived suppressor cells. In blood stream, whole blood cells and endothelail cells exist in vivo no in vitro. We demostrated that endothelial cells are required for metastatic cancer cell-induced CD26 upregulation of innate immune cells, not via whole blood cells. Furthermore, we observed that metastatic cancer cells stimulated endothelial cells secreting conditioned medium to induce CD26 upregulation and cytotoxic suppression of innate immune cells. Innate immune cells activated via several of cytokine and chemokine. Therefore, we used the flowcytomix bead-based protein detection system to analyse the condition medium and observed that IL-6 upregualtion in C.M..

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