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...

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Bibliographic Details
Published inTrends in immunology Vol. 42; no. 10; pp. 849 - 851
Main Authors Cao, Huan, Vickers, Mark A.
Format Journal Article
LanguageEnglish
Published Oxford Elsevier Ltd 01.10.2021
Elsevier Limited
Subjects
Adaptive immunity
Anemia
Binding sites
damage-associated molecular pattern
Erythrocytes
Hemoglobin
high-mannose glycans
Immune system
Immunity (Disease)
Infections
Innate immunity
Ligands
Malaria
Mannose
Mutation
Oxidative stress
Parasites
pathogen-associated molecular pattern
Pathogens
Phagocytosis
Plasmodium falciparum
Polysaccharides
Proteins
Sickle cell disease
Spleen
Vector-borne diseases
phagocytosis
damage-associated molecular pattern
high-mannose glycans
malaria
pathogen-associated molecular pattern
oxidative stress
sickle cell disease
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Summary: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.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1471-4906
1471-4981
DOI:10.1016/j.it.2021.08.008