期刊
CELL HOST & MICROBE
卷 19, 期 2, 页码 194-203出版社
CELL PRESS
DOI: 10.1016/j.chom.2016.01.009
关键词
-
资金
- Ministerio de Ciencia e Innovacion, Spain
- National Institutes of Health (NIH) [5T32AI100853-03]
- Burroughs Wellcome Fund Award for Investigators in the Pathogenesis of Infectious Disease
- Dana Foundation
- Labex GR-EX
- NIH National Institute of Allergy and Infectious Diseases [U19AI089676-01S1]
Plasmodium species, the parasitic agents of malaria, invade erythrocytes to reproduce, resulting in erythrocyte loss. However, a greater loss is caused by the elimination of uninfected erythrocytes, sometimes long after infection has been cleared. Using a mouse model, we found that Plasmodium infection induces the generation of anti-self antibodies that bind to the surface of uninfected erythrocytes from infected, but not uninfected, mice. These antibodies recognize phosphatidylserine, which is exposed on the surface of a fraction of uninfected erythrocytes during malaria. We find that phosphatidylserine-exposing erythrocytes are reticulocytes expressing high levels of CD47, a do-not-eat-me'' signal, but the binding of anti-phosphatidylserine antibodies mediates their phagocytosis, contributing to anemia. In human patients with late postmalarial anemia, we found a strong inverse correlation between the levels of anti-phosphatidylserine antibodies and plasma hemoglobin, suggesting a similar role in humans. Inhibition of this pathway may be exploited for treating malarial anemia.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据