Oxidative stress, malaria, sickle cell disease, and innate immunity

Plasmodium falciparum shields from adaptive immunity in erythrocytes, but how might the innate immune system recognize infected cells? Replication by the parasite results in oxidative stress, causing surface expression of high-mannose glycans. These can act as pathogen associated molecular patterns to stimulate phagocytosis in the spleen and the sickle cell allele enhances these responses.

Automated summary

Plasmodium falciparum evades adaptive immunity in erythrocytes, but the innate immune system can recognize infected cells through the expression of high-mannose glycans induced by oxidative stress caused by parasite replication. These glycans act as pathogen associated molecular patterns, stimulating phagocytosis in the spleen, with enhanced responses in individuals with the sickle cell allele.