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恶性疟原虫和间日疟原虫感染中的免疫调节改变。

Immunoregulatory alterations in Plasmodium falciparum and Plasmodium vivax infections.

作者信息

Merino F, Layrisse Z, Godoy G, Volcán G

出版信息

Trop Med Parasitol. 1986 Sep;37(3):241-4.

PMID:2947313
Abstract

Studies on the immune function of patients with acute Plasmodium vivax or P. falciparum infections were performed. All subjects were residing in recent malaria endemic areas of Venezuela. Lymphopenia, reduction of peripheral blood T-lymphocytes positive for monoclonal antibody OKT4 (T helper) a decrease of in vitro mitogenic proliferative response and natural killer cell activity were observed. Serum lymphocytotoxic antibodies reactive at 37 degrees C were detected in both groups of patients as well as serum autoantibodies. The possible role of lymphocytotoxic autoantibodies in the etiology of the T-lymphocyte depletion and acquired immunological perturbations in human malaria is discussed.

摘要

对急性间日疟或恶性疟患者的免疫功能进行了研究。所有受试者均居住在委内瑞拉近期的疟疾流行地区。观察到淋巴细胞减少、外周血中对单克隆抗体OKT4呈阳性的T淋巴细胞(辅助性T细胞)减少、体外有丝分裂原增殖反应降低以及自然杀伤细胞活性降低。在两组患者中均检测到在37摄氏度时有反应的血清淋巴细胞毒性抗体以及血清自身抗体。讨论了淋巴细胞毒性自身抗体在人类疟疾中T淋巴细胞耗竭和获得性免疫紊乱病因中的可能作用。

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1
Immunoregulatory alterations in Plasmodium falciparum and Plasmodium vivax infections.恶性疟原虫和间日疟原虫感染中的免疫调节改变。
Trop Med Parasitol. 1986 Sep;37(3):241-4.
2
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Plasmodium falciparum and P. vivax gametocyte-specific exoantigens stimulate proliferation of TCR gammadelta+ lymphocytes.恶性疟原虫和间日疟原虫配子体特异性外抗原刺激TCRγδ+淋巴细胞增殖。
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引用本文的文献

1
Multispecies Plasmodium infections of humans.人类的多种疟原虫感染。
J Parasitol. 1999 Feb;85(1):12-8.
2
The gamma/delta T-cell response to Plasmodium falciparum malaria in a population in which malaria is endemic.在疟疾流行地区人群中,γ/δ T细胞对恶性疟原虫疟疾的反应。
Infect Immun. 1996 Oct;64(10):4359-62. doi: 10.1128/iai.64.10.4359-4362.1996.
3
Cytotoxicity of human natural killer (NK) cell subsets for Plasmodium falciparum erythrocytic schizonts: stimulation by cytokines and inhibition by neomycin.人类自然杀伤(NK)细胞亚群对恶性疟原虫红细胞内期裂殖体的细胞毒性:细胞因子的刺激作用和新霉素的抑制作用
Clin Exp Immunol. 1991 Oct;86(1):22-9. doi: 10.1111/j.1365-2249.1991.tb05768.x.