Lymphocyte migration into the CNS modelled in vitro

Male, David; Pryce, Gareth; Linke, A; Rahman, Jameel

doi:10.1016/0165-5728(92)90130-d

Cited by 48 publications

(29 citation statements)

References 6 publications

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“…IFN-␥ and critically regulate the recruitment of T cells to the brain (21,(32)(33)(34)(35)(36)(37). Thus, a depletion of cytokine-producing T cells may result in an impaired recruitment of T cells to the brain via the reduced expression of cell adhesion molecules on brain vessel endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Protective Immunosurveillance of the Central Nervous System by Listeria-Specific CD4 and CD8 T Cells in Systemic Listeriosis in the Absence of Intracerebral Listeria

Kwok

Miletić

Lütjen

et al. 2002

The Journal of Immunology

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The invasion of the CNS by pathogens poses a major risk for damage of the highly vulnerable brain. The aim of the present study was to analyze immunological mechanisms that may prevent spread of infections to the CNS. Intraperitoneal application of Listeria monocytogenes to mice induced infection of the spleen, whereas pathogens remained absent from the brain. Interestingly, Listeria-specific CD4 and CD8 T cells homed to the brain and persisted intracerebrally for at least 50 days after both primary and secondary infection. CD4 and CD8 T cells resided in the leptomeninges, in the choroid plexus, and, in low numbers, in the brain parenchyma. CD4 and CD8 T cells isolated from the brain early after infection (day 7) were characterized by an activated phenotype with spontaneous IFN-γ production, whereas at a later stage of infection (day 28) restimulation with Listeria-specific peptides was required for the induction of IFN-γ production by CD4 and CD8 T cells. In contrast to splenic T cells, T cells in the brain did not exhibit cytotoxic activity. Adoptively transferred T cells isolated from the brains of Listeria-infected mice reduced the bacterial load in cerebral listeriosis. The frequency of intracerebral Listeria-specific T cells was partially regulated by the time of exposure to Listeria and cross-regulated by CD4 and CD8 T cells. Collectively, these data reveal a novel T cell-mediated pathway of active immunosurveillance of the CNS during bacterial infections.

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Section: Discussionmentioning

confidence: 99%

Protective Immunosurveillance of the Central Nervous System by Listeria-Specific CD4 and CD8 T Cells in Systemic Listeriosis in the Absence of Intracerebral Listeria

Kwok

Miletić

Lütjen

et al. 2002

The Journal of Immunology

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“…The absence of elevated IL-1␤ transcripts in infected HBMEC was already observed in meningeal cells (64). Other infection-induced HBMEC genes specifically involved in neutrophil recruitment were the ICAM-1 gene, which, when up-regulated, leads to enhanced adhesion of neutrophils to the brain endothelium (14,15,32).…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Pattern in Human Brain Endothelial Cells in Response to Neisseria meningitidis

et al. 2007

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To extend our knowledge of target proteins in endothelial cells infected with the meningitis-causing pathogen Neisseria meningitidis, we characterized the interaction between the bacterial and human brain microvascular endothelial cell (HBMEC) monolayers. By use of human cDNA microarrays, transcriptional analysis revealed distinct responses to 4 and 8 h of infection. We also addressed the question of whether the major virulence factor of meningococci, i.e., the capsule, influences the host cell response. Of the 1,493 (at 4 h postinfection) and 1,246 (at 8 h postinfection) genes with altered expression upon bacterial contact, about 49.4% and 45%, respectively, depended on capsule expression. In particular, we identified an increase of expression for genes encoding proteins involved in bacterial adhesion and invasion. High levels of apoptosis-related gene (bad, bak, asp, and immediate-early response gene 1) expression could also be detected in infected cells. Further analyses confirmed that HBMECs displayed several hallmarks of apoptosis in response to N. meningitidis infection, namely, phosphatidylserine translocation and activation of caspase 3 and AMP-activated protein kinase ␣. Moreover, several differentially regulated genes not previously known to respond to meningococcal infection were identified. Of these, genes encoding cell adhesion proteins (CD44, CD98, and CD99), genes involved in downstream signaling of integrins (integrin-linked kinase, mitogen-activated protein kinase kinase 1, and mitogen-activated protein kinase kinase kinase 10) as well as negative regulators of these pathways (dualspecificity phosphatases 1, 5, and 14 and G protein pathway suppressor 2), and genes involved in cytoskeleton reorganization (those encoding Arp2/3, p34-arc, actinin alpha 1, vasodilatator-stimulated protein, and Wiskott-Aldrich syndrome protein) were the most prominent. This global transcriptional analysis creates a new platform for further molecular and cellular analysis of the interaction between N. meningitidis and target cells.

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“…In addition, IL-8 stimulates neutrophil respiratory burst, degranulation, and adherence to endothelial cells. Other GBS-induced HBMEC genes related specifically to CNS neutrophil recruitment were ICAM-1, which when upregulated leads to the enhanced adhesion of neutrophils to the brain endothelium (26), and GM-CSF, which increases neutrophil migration across brain endothelium (27). The programmed cell death of neutrophils can be delayed by GM-CSF (28-30), a process that was recently shown to be mediated through the specific induction of the antiapoptotic factor Mcl-1 (31), whose gene product was also elevated in our experiments.…”

Section: Discussionmentioning

confidence: 99%

Group B streptococcal β-hemolysin/cytolysin activates neutrophil signaling pathways in brain endothelium and contributes to development of meningitis

Doran¹,

Liu²,

Nizet³

2003

J. Clin. Invest.

198

173

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Lymphocyte migration into the CNS modelled in vitro

Cited by 48 publications

References 6 publications

Protective Immunosurveillance of the Central Nervous System by Listeria-Specific CD4 and CD8 T Cells in Systemic Listeriosis in the Absence of Intracerebral Listeria

Protective Immunosurveillance of the Central Nervous System by Listeria-Specific CD4 and CD8 T Cells in Systemic Listeriosis in the Absence of Intracerebral Listeria

Gene Expression Pattern in Human Brain Endothelial Cells in Response to Neisseria meningitidis

Group B streptococcal β-hemolysin/cytolysin activates neutrophil signaling pathways in brain endothelium and contributes to development of meningitis

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