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題 名 | Non-Specific Immunosuppression in Jirds Acutely Infected with Brugia pahangi=Brugia pahangi 急性感染沙鼠之非特異性免疫抑制 |
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作 者 | 林大盛; | 書刊名 | 國立臺灣大學農學院研究報告 |
卷 期 | 34:4 1994.12[民83.12] |
頁 次 | 頁360-372 |
分類號 | 437.245 |
關鍵詞 | 抗原; 細胞分裂刺激物; 免疫抑制; 沙鼠; 絲蟲; 脾細胞; 淋巴結細胞; 調節細胞; 抑制細胞; Antigen; Mitogen; Immunosuppression; Jird; Filaria; Spleen cell; Lymph node cell; Regulatory cell; Suppressor cell; |
語 文 | 英文(English) |
中文摘要 | 以前研究指出,不論急性或慢性Brugia pahangi感染,皆只對再次感染的 仔蟲產生低度免疫反應。早期B. pahangi感染產生的免疫抑制尤其有趣,因為此種 低反應狀態有利感染仔蟲在宿主內存活。抗原特異性及非特異免疫抑制兩者,在 B.pahangi急性感染沙鼠皆有發現。前者會被加以研究,並發現是由對尼龍絲有附 著力之抗原特異性調節細胞所導致。因此,本研究乃要証明在急性感染亦存在有 非特異性調節細胞。結果指出,沙鼠之脾細胞在B.pahangi感染後之第二、四、及 十四天,或淋巴結細胞在感染後第二天,可抑制正常細胞對phytohemagglutinin之 反應。對lipopolysaccharide之反應,脾或淋巴結細胞另在感染後第二天有抑制作 用。相反的,脾細胞在感染後第七夭卻增強正當細胞對lipopolysaccharide之反應。 在調節細胞偵測方面,concanavalin A可刺激並拉大沒感染或有感染細胞中調節細 胞之族群。雖然如此,B.pa力an矽"抗原只能刺激感染細胞中的調節細胞。對於組 織胺,補體,前列腺素,T抑制細胞,巨噬細胞或第二型幫助T細胞可能參與非 特異性免疫抑制,赤在此討論之。 |
英文摘要 | Previous studies have shown that existing acute or chronicfilarial infection may cause immunologic hypo-responsiveness to thedeveloping larvae of subsequent Brugia pahangi infection. Theimmunosuppression occurred in the early stage of B. pahangiinfection is most interesting, because this hypo-responsiveness statusfavors the survival of infective larvae in the host. Bothantigen-specific and non-specific immunosuppression has beenobserved in B. pahangi -acutely infected jirds. The former has beenexamined and found to be mediated by antigen-specific, nylon wooladherent regulatory cells. Hence, the present study was designed todemonstrate that, in a.cute infection, there were also the presence ofnon-specific regulatory (suppressor) cells. The results indicated thatspleen cells from B. pahangi -infected jirds at 2, 4, and 14 dayspost-infection or lymph node cells at 2 days post-infection were ableto suppress the reactivity of normal cells to phytohemagglutinin. Asfar as the reactivity to lipopolysaccharide was concerned, both spleenand lymph node cells only at 2 days post-infection had suppressiveeffect. In contrast, spleen cells on day 7 after infection amplified thereactivity of normal cells to lipopolysacch'aride. In regulatory cellassay, concanavalin A was able to stimulate and expand theregulatory cell population in either un-infected or infected cells.However, B. pahangi antigens only stimulated regulatory cells ininfected cell population. The possibility of the involvement ofhistamine, complements, prostaglandins, T suppressor cells,macrophages, or T helper type 2 cells in the non-specific immunosuppression is also discussed. |
本系統中英文摘要資訊取自各篇刊載內容。