| Summary: | 碩士 === 國立成功大學 === 生物化學暨分子生物學研究所 === 101 === 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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