磷脂酰丝氨酸
生物
抗体
贫血
吞噬作用
疟疾
间隙
血红蛋白
免疫学
病毒学
生物化学
磷脂
内科学
医学
膜
泌尿科
作者
Cristina Fernández-Arias,Juan Rivera-Correa,Julio Gállego-Delgado,Rachel M. Rudlaff,Clemente Fernandez,Camille Roussel,Anton Götz,Sandra González,Akshaya Kumar Mohanty,Sanjib Mohanty,Samuel C. Wassmer,Pierre Buffet,Papa Alioune Ndour,Ana Rodrı́guez
标识
DOI:10.1016/j.chom.2016.01.009
摘要
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.
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