惡性瘧原蟲175KDa紅細(xì)胞結(jié)合抗原與其受體相互作用分子機制的研究
發(fā)布時間:2018-05-26 15:51
本文選題:中醫(yī)藥 + 惡性瘧原蟲EBA-175; 參考:《第一軍醫(yī)大學(xué)》2005年碩士論文
【摘要】:一、研究背景與目的 瘧疾是危害人類健康的蟲媒傳染病,廣泛流行于熱帶和亞熱帶一些發(fā)展中國家。近年來,由于瘧原蟲抗藥性和蚊媒耐藥性的日益增強和廣泛擴散,加之一些現(xiàn)代經(jīng)濟和社會因素的影響,使瘧疾(尤其是惡性瘧原蟲)的流行有復(fù)燃趨勢,急性感染病人越來越多,而可供選擇的廉價、有效的化療藥物越來越少,從而使瘧疾的防治面臨嚴(yán)峻挑戰(zhàn)。 惡性瘧原蟲的175-KDa紅細(xì)胞結(jié)合抗原(EBA-175)自1985年由Camus和Hadley首次報道以來,經(jīng)大量免疫學(xué)實驗研究和流行病學(xué)調(diào)查證明:其既是瘧疾疫苗的候選抗原,也是瘧疾的特異診斷抗原。其位于裂殖子尖端微線體,與血型糖蛋白A(GPA)分子上o~-糖苷鍵寡糖的Neu5Ac(α2-3)-Gal決定簇結(jié)合,能夠有效抑制裂殖子入侵紅細(xì)胞。EBA-175與受體GPA結(jié)合點是位于氨基末端富含半光氨酸的Ⅱ區(qū),該區(qū)F2結(jié)構(gòu)域的抗體能夠阻斷該分子與GPA的反應(yīng)并能抑制裂殖子入侵紅細(xì)胞,表明該區(qū)域?qū)Ο懺x的致病具有功能重要性。這就為瘧疾的發(fā)病機制提出了新的學(xué)說,亦為其預(yù)防和治療提出了新的契入點。 自上世紀(jì)50年代以來,我國在中醫(yī)藥防治瘧疾方面取得了豐碩的成果,尤其是應(yīng)用青蒿素治療惡性瘧疾取得優(yōu)良療效的研究。為中醫(yī)藥抗瘧鋪開了光明
[Abstract]:I. the background and purpose of the research Malaria is an insect-borne infectious disease that is harmful to human health and is widely prevalent in some developing countries in the tropics and subtropics. In recent years, the increasing and widespread spread of malaria resistance and mosquito resistance, coupled with the impact of modern economic and social factors, has led to a resurgence of malaria, especially Plasmodium falciparum, There are more and more patients with acute infection, and the cheap and effective chemotherapeutic drugs available are becoming less and less, which makes the prevention and treatment of malaria face severe challenges. The 175-KDa erythrocyte binding antigen (EBA-175) of Plasmodium falciparum was first reported by Camus and Hadley in 1985. It has been proved by a large number of immunological experiments and epidemiological investigations that it is not only a candidate antigen for malaria vaccine, but also a specific diagnostic antigen for malaria. It is located at the tip of merozoite and binds to Neu5AcA (偽 2-3)-Gal determinant) of oligosaccharide on the blood group glycoprotein Agna. It can effectively inhibit the merozoite invasion of erythrocyte. EBA-175 and receptor GPA binding site is located at the amino end of the 鈪,
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