ArticleThe Journal of biological chemistry2013
Experimental cerebral malaria develops independently of endothelial expression of intercellular adhesion molecule-1 (icam-1).
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- The role of parasite-derived vesicles in modulating neutrophil responses in emerging human babesiosis.Emerging microbes & infections · 2026Article
- Carbohydrates: Binding Sites and Potential Drug Targets for Neural-Affecting Pathogens.Advances in neurobiology · 2023Article
- Cerebral Malaria: Current Clinical and Immunological Aspects.Frontiers in immunology · 2022Review
- Cerebral malaria induced byFrontiers in cellular and infection microbiology · 2022Review
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Parasite Recognition and Signaling Mechanisms in Innate Immune Responses to Malaria.Frontiers in immunology · 2018Review
- Doxycycline inhibits experimental cerebral malaria by reducing inflammatory immune reactions and tissue-degrading mediators.PloS one · 2018Article
- Endothelial-Leukocyte Interaction in Severe Malaria: Beyond the Brain.Mediators of inflammation · 2015Review
- Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier.PLoS pathogens · 2014Article
- ICAM-1: isoforms and phenotypes.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Cerebral malaria (CM) is a severe clinical complication of Plasmodium falciparum malaria infection and is characterized by a high fatality rate and neurological damage. Sequestration of parasite-infected red blood cells in brain microvasculature utilizes host- and parasite-derived adhesion molecules and is an important factor in the development of CM. ICAM-1, an alternatively spliced adhesion molecule, is believed to be critical on endothelial cells for infected red blood cell sequestration in CM. Using ICAM-1 mutant mice, we found that the full-length ICAM-1 isoform is not required for development of murine experimental CM (ECM) and that ECM phenotype varies with the combination of ICAM-1 isoforms expressed. Furthermore, we observed development of ECM in transgenic mice expressing ICAM-1 only on leukocytes, indicating that endothelial cell expression of this adhesion molecule is not required for disease pathogenesis. We propose that ICAM-1-dependent cellular aggregation, independent of ICAM-1 expression on the cerebral microvasculature, contributes to ECM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.