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年轻生命因 B 细胞衰竭而消逝:我们对疟疾抗体反应的了解。

Young lives lost as B cells falter: what we are learning about antibody responses in malaria.

机构信息

Laboratory of Immunogenetics, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA.

出版信息

J Immunol. 2013 Apr 1;190(7):3039-46. doi: 10.4049/jimmunol.1203067.

Abstract

Plasmodium falciparum malaria remains a major public health threat for which there is no licensed vaccine. Abs play a key role in malaria immunity, but Ab-mediated protection is only acquired after years of repeated infections, leaving children in endemic areas vulnerable to severe malaria and death. Many P. falciparum Ags are extraordinarily diverse and clonally variant, which likely contribute to the inefficient acquisition of protective Abs. However, mounting evidence suggests that there is more to the story and that infection-induced dysregulation of B cell function also plays a role. We herein review progress toward understanding the B cell biology of P. falciparum infection, focusing on what has been learned from population-based studies in malaria-endemic areas. We suggest ways in which advances in immunology and genomics-based technology can further improve our understanding of the B cell response in malaria and perhaps illuminate new pathways to the development of effective vaccines.

摘要

恶性疟原虫疟疾仍然是一个主要的公共卫生威胁,目前还没有许可的疫苗。抗体在疟疾免疫中起着关键作用,但抗体介导的保护只有在多年的反复感染后才能获得,这使得流行地区的儿童容易受到严重疟疾和死亡的影响。许多恶性疟原虫抗原非常多样化和克隆变异,这可能导致保护性抗体的获得效率低下。然而,越来越多的证据表明,情况并非如此,感染诱导的 B 细胞功能失调也起作用。本文综述了在理解恶性疟原虫感染的 B 细胞生物学方面的进展,重点介绍了从疟疾流行地区的基于人群的研究中获得的认识。我们提出了如何利用免疫学和基于基因组学的技术进步来进一步提高我们对疟疾中 B 细胞反应的理解,并可能为开发有效疫苗开辟新途径。

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