ArticleImmunology1997
Expression of major histocompatibility complex antigens on mouse brain microvascular endothelial cells in relation to susceptibility to cerebral malaria.
Article in Immunology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Endothelial microparticles interact with and support the proliferation of T cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- A population of CD4Clinical & translational immunology · 2020Article
- Transcriptome analysis of human brain microvascular endothelial cells response to Neisseria meningitidis and its antigen MafA using RNA-seq.Scientific reports · 2019Article
- Perivascular Arrest of CD8+ T Cells Is a Signature of Experimental Cerebral Malaria.PLoS pathogens · 2015Article
- The brain microvascular endothelium supports T cell proliferation and has potential for alloantigen presentation.PloS one · 2013Article
- Endothelial cells potentiate interferon-γ production in a novel tripartite culture model of human cerebral malaria.PloS one · 2013Article
- Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Peroxisome proliferator activating receptor (PPAR) in cerebral malaria (CM): a novel target for an additional therapy.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2011Review
- Predominance of interferon-related responses in the brain during murine malaria, as identified by microarray analysis.Infection and immunity · 2008Article
- Detection of a new cerebral malaria susceptibility locus, using CBA mice.Immunogenetics · 2004Article
- Pathogenesis of cerebral malaria: recent experimental data and possible applications for humans.Clinical microbiology reviews · 2001Review
- Immunopathology of cerebral malaria: morphological evidence of parasite sequestration in murine brain microvasculature.Infection and immunity · 2000Article
- Interferon-gamma receptor-mediated but not tumor necrosis factor receptor type 1- or type 2-mediated signaling is crucial for the activation of cerebral blood vessel endothelial cells and microglia in murine Toxoplasma encephalitis.The American journal of pathology · 1999Article
- Cerebral endothelial activation and signal transduction mechanisms during inflammation and infectious disease.The American journal of pathology · 1999Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The physiopathology of experimental cerebral malaria (CM), an acute neurological complication of Plasmodium berghei ANKA (PbA) infection, involves interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha), two cytokines that are known to modulate major histocompatibility complex (MHC) molecule expression. The aim of this study was to evaluate whether the genetic susceptibility to CM is related to the constitutive or IFN-gamma-induced expression of MHC molecules on brain microvessels. To this end, brain microvascular endothelial cells (B-MVEC) were isolated from CM-susceptible (CM-S, CBA/J) and resistant (CM-R, BALB/c) mice. By flow cytometry, we found that less than 5% of CM-S B-MVEC constitutively expressed MHC class I molecules, in contrast to up to 90% of CM-R B-MVEC. Upon stimulation with IFN-gamma, the percentage of positive cells for MHC class I molecules in CM-S B-MVEC became comparable to CM-R B-MVEC, but a higher fluorescence intensity existed on CM-S B-MVEC compared with CM-R B-MVEC. MHC class II molecules were not constitutively expressed on B-MVEC from either strain. IFN-gamma-induced expression of MHC class II (I-A, I-E) molecules was significantly higher in CM-S than CM-R B-MVEC both in percentage of positive cells and fluorescence intensity. These data demonstrate that absent or low MHC class I and higher inducibility of MHC class II expression on B-MVEC are associated with the genetic susceptibility to CM.
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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.