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.
Keywords: damage-associated molecular pattern; high-mannose glycans; malaria; oxidative stress; pathogen-associated molecular pattern; phagocytosis; sickle cell disease.
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