林大盛2006-07-262018-07-092006-07-262018-07-092000http://ntur.lib.ntu.edu.tw//handle/246246/28686維生素E 為一主要的脂溶性細胞膜抗 氧化物，可保護細胞免受自由基之破壞。 另外，維生素E 亦可影響細胞內生化反 應，但作用機制並不清楚。維生素E 對於 培養的淋巴球有保護與刺激作用，但原因 並非是單純的由於減低細胞膜之lipid peroxidation。有證據指出，維生素E 亦可 能為免疫調控物質(immunomodulator)，對 維持正常的免疫功能很重要。在探討老化 的研究發現：年輕時以Th1 型免疫反應為 主，而年老時免疫反應轉而偏向Th2 型免 疫反應。由於維生素E 有抗老化作用，又 因為維生素E 可促使IL-2 及IFN-g之產 生，吾人因而推論維生素E 之抗老化作用 可能是因促進了Th1 型免疫反應所致。故 維生素E 很可能為Th1 型免疫反應之一種 調控物質。Th1 型免疫反應主要藉由Th1 細胞分泌cytokines 執行，如IL-2、IFN-g 等。去年的國科會計畫以探討維生素E 調 控淋巴球的反應為主，初步結果支持維生 素E 可刺激淋巴球。但是，另外有證據指 出：以維生素E 處理過之巨噬細胞和淋巴 球培養在一起時，可增進淋巴球對mitogens 及維生素E 之反應。故維生素E 可能刺激 巨噬細胞釋放出monokines 如IL-1，以影 響淋巴球的反應。另外已知，巨噬細胞亦 可分泌IL-12，有助於促進Th1 型免疫反 應。吾人因此提出假說：維生素E 之促進 Th1 型免疫反應，除了可能直接調控淋巴 球外，維生素E 尚可藉由調控巨噬細胞， 影響其功能，而促使淋巴球免疫反應趨於 Th1 型。結果證實維生素E 在 lipopolysaccharide (LPS) 刺激下可增強巨 噬細胞之sarcoma cells 破壞能力，且巨噬 細胞以維生素E 併以適當濃度之LPS 處理 後與淋巴細胞培養可促使後者增生。然而 以enzyme linked immunosorbent assay (ELISA) 卻無法證實IL-1 分泌有增加。進 一步以enzyme-linked immunospot (ELISPOT) 法亦無法證實維生素E 及LPS 處理過的巨噬細胞能刺激以Th1 型為主的 淋巴球免疫反應。Vitamin E (VE) is the major lipid soluble membrane antioxidant which protects the cell from the damage by free radicals. VE can influence intracellular activity, though these mechanisms are not clear. In addition, VE can protect and stimulate cultured lymphocytes and this is not simply due to the decrease of membrane lipid peroxidation. It is evident that VE can act as an immunomodulator which is essential in maintaining normal immunological activity. The investigations on aging show that Th1- type immune response is dominant when one is young and the immune response is switching to Th2 when one is getting old. Because VE has anti-aging effect and also because VE can induce IL-2 and IFN-g production, we conclude that anti-aging effect of VE is due to it’s enhancement of Th1-type immune response. Thus, VE can be an immunomodulator for Th1-type immune response whose effects are due to the release of cytokines: like IL-2, IFN-g by Th1 cells. The NSC project last year studied the modulation of lymphocytes by VE. The preliminary results support VE as a lymphocyte stimulator. However, other evidences indicate that the responsiveness of lymphocytes to mitogens and VE is enhanced when lymphocytes are cultured with VEpretreated macrophages. Therefore, VE may stimulate macrophages to release monokines like IL-1 influencing lymphocyte response. Also, it is known that macrophages can release IL-12 which promotes Th1-type immune response. Therefore, it is hypothesized that in addition to direct lymphocyte modulation, VE can modulate macrophages influencing their functions which guides lymphocyte towards Th1 immune response. The results showed that in the presence of LPS, VE could enhance sarcoma cell-killing ability of macrophages. Also, macrophages, after treatment with VE and LPS, could enhance the proliferation of co-cultured lymphocytes. However, macrophage IL-1 secretion was not proved to be enhanced by ELISA, and lymphocyte responses were not dominated by Th1-type cytokines as measured by ELISPOT.application/pdf52946 bytesapplication/pdfzh-TW國立臺灣大學獸醫學系暨研究所維生素E免疫調控巨噬細胞細胞素vitamin Eimmunomodulationmacrophagecytokinereporthttp://ntur.lib.ntu.edu.tw/bitstream/246246/28686/1/892313B002078.pdf