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本文引用的文献

1
Negative epistasis between the malaria-protective effects of alpha+-thalassemia and the sickle cell trait.α+地中海贫血的疟疾保护作用与镰状细胞性状之间的负上位性。
Nat Genet. 2005 Nov;37(11):1253-7. doi: 10.1038/ng1660. Epub 2005 Oct 16.
2
Normal functional capacity in circulating myeloid and plasmacytoid dendritic cells in patients with chronic hepatitis C.慢性丙型肝炎患者循环髓样和浆细胞样树突状细胞的正常功能能力。
J Infect Dis. 2005 Aug 1;192(3):497-503. doi: 10.1086/431523. Epub 2005 Jun 27.
3
Sickle cell trait and the risk of Plasmodium falciparum malaria and other childhood diseases.镰状细胞性状与恶性疟原虫疟疾及其他儿童疾病的风险
J Infect Dis. 2005 Jul 1;192(1):178-86. doi: 10.1086/430744. Epub 2005 May 31.
4
An immune basis for malaria protection by the sickle cell trait.镰状细胞性状对疟疾的免疫保护基础。
PLoS Med. 2005 May;2(5):e128. doi: 10.1371/journal.pmed.0020128. Epub 2005 May 31.
5
The sickle cell trait is associated with enhanced immunoglobulin G antibody responses to Plasmodium falciparum variant surface antigens.镰状细胞性状与针对恶性疟原虫变异表面抗原的免疫球蛋白G抗体反应增强有关。
J Infect Dis. 2005 May 15;191(10):1631-8. doi: 10.1086/429832. Epub 2005 Apr 12.
6
Both heterozygous and homozygous alpha+ thalassemias protect against severe and fatal Plasmodium falciparum malaria on the coast of Kenya.在肯尼亚海岸,杂合子和纯合子α+地中海贫血都能预防严重和致命的恶性疟原虫疟疾。
Blood. 2005 Jul 1;106(1):368-71. doi: 10.1182/blood-2005-01-0313. Epub 2005 Mar 15.
7
Toll-like receptor 9 mediates innate immune activation by the malaria pigment hemozoin.Toll样受体9介导疟色素疟原虫血红素引起的天然免疫激活。
J Exp Med. 2005 Jan 3;201(1):19-25. doi: 10.1084/jem.20041836.
8
Induction of proinflammatory responses in macrophages by the glycosylphosphatidylinositols of Plasmodium falciparum: cell signaling receptors, glycosylphosphatidylinositol (GPI) structural requirement, and regulation of GPI activity.恶性疟原虫糖基磷脂酰肌醇对巨噬细胞促炎反应的诱导:细胞信号受体、糖基磷脂酰肌醇(GPI)结构要求及GPI活性调节
J Biol Chem. 2005 Mar 4;280(9):8606-16. doi: 10.1074/jbc.M413541200. Epub 2004 Dec 28.
9
Induction of proinflammatory responses in macrophages by the glycosylphosphatidylinositols of Plasmodium falciparum: the requirement of extracellular signal-regulated kinase, p38, c-Jun N-terminal kinase and NF-kappaB pathways for the expression of proinflammatory cytokines and nitric oxide.恶性疟原虫糖基磷脂酰肌醇诱导巨噬细胞促炎反应:促炎细胞因子和一氧化氮表达对细胞外信号调节激酶、p38、c-Jun氨基末端激酶和核因子κB信号通路的需求
J Biol Chem. 2005 Mar 4;280(9):8617-27. doi: 10.1074/jbc.M413539200. Epub 2004 Dec 15.
10
Malaria and nutritional status in children living on the coast of Kenya.肯尼亚沿海地区儿童的疟疾与营养状况
Am J Clin Nutr. 2004 Dec;80(6):1604-10. doi: 10.1093/ajcn/80.6.1604.

患有α+地中海贫血和镰状细胞性状的肯尼亚健康儿童外周血髓细胞频率

Frequencies of peripheral blood myeloid cells in healthy Kenyan children with alpha+ thalassemia and the sickle cell trait.

作者信息

Urban Britta C, Shafi Mohammed J, Cordery Damien V, Macharia Alex, Lowe Brett, Marsh Kevin, Williams Thomas N

机构信息

Centre for Clinical Vaccinology and Tropical Medicine, Nuffield Department of Clinical Medicine, Oxford University, Churchill Hospital, Oxford, United Kingdom.

出版信息

Am J Trop Med Hyg. 2006 Apr;74(4):578-84.

PMID:16606987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2742660/
Abstract

The high frequencies of both alpha+ thalassemia and the sickle cell trait (hemoglobin AS [HbAS]) found in many tropical populations are thought to reflect selection pressure from Plasmodium falciparum malaria. For HbAS, but not for alpha+ thalassemia, protection appears to be mediated by the enhanced phagocytic clearance of ring-infected erythrocytes. We have investigated the genotype-specific distributions of peripheral blood leukocyte populations in two groups of children living on the coast of Kenya: a group of healthy P. falciparum parasite-negative children sampled at cross-sectional survey during a period of low malaria transmission, and a group of children attending the hospital with acute malaria. We report distinctive distributions of peripheral blood myeloid dendritic cells and monocytes in children with alpha+ thalassemia and HbAS during healthy periods and disease, and suggest ways in which these might relate to the mechanisms of protection afforded by these conditions.

摘要

在许多热带人群中发现的α+地中海贫血和镰状细胞性状(血红蛋白AS [HbAS])的高频率被认为反映了恶性疟原虫疟疾的选择压力。对于HbAS,而不是α+地中海贫血,保护作用似乎是由被环状感染红细胞的吞噬清除增强介导的。我们调查了肯尼亚海岸两组儿童外周血白细胞群体的基因型特异性分布:一组是在疟疾传播低的时期进行横断面调查时抽取的健康恶性疟原虫寄生虫阴性儿童,另一组是因急性疟疾住院的儿童。我们报告了α+地中海贫血和HbAS儿童在健康期和患病期间外周血髓样树突状细胞和单核细胞的独特分布,并提出了这些分布可能与这些病症所提供的保护机制相关的方式。