Homing to central nervous system vasculature by antigen-specific lymphocytes. I. Localization of 14C-labeled cells during acute, chronic, and relapsing experimental allergic encephalomyelitis.
about
Fluids and barriers of the CNS establish immune privilege by confining immune surveillance to a two-walled castle moat surrounding the CNS castleThe voltage-gated potassium channel Kv1.3 is highly expressed on inflammatory infiltrates in multiple sclerosis brainIncreased expression of ICAM-1, VCAM-1, MCP-1, and MIP-1 alpha by spinal perivascular macrophages during experimental allergic encephalomyelitis in rats.CC chemokine receptor 2 is critical for induction of experimental autoimmune encephalomyelitisAbsence of monocyte chemoattractant protein 1 in mice leads to decreased local macrophage recruitment and antigen-specific T helper cell type 1 immune response in experimental autoimmune encephalomyelitisLocalizing central nervous system immune surveillance: meningeal antigen-presenting cells activate T cells during experimental autoimmune encephalomyelitis.T-cell receptor (TCR) usage in Lewis rat experimental autoimmune encephalomyelitis: TCR beta-chain-variable-region V beta 8.2-positive T cells are not essential for induction and course of disease.A lymphocyte homing receptor (L-selectin) mediates the in vitro attachment of lymphocytes to myelinated tracts of the central nervous system.CCL22 regulates experimental autoimmune encephalomyelitis by controlling inflammatory macrophage accumulation and effector function.Molecular control of physiological and pathological T-cell recruitment after mouse spinal cord injuryDelta-like ligand 4 regulates central nervous system T cell accumulation during experimental autoimmune encephalomyelitis.Experimental autoimmune encephalomyelitis (EAE) in CCR2(-/-) mice: susceptibility in multiple strainsBreakdown of the blood-retinal barrier induced by activated T cells of nonneural specificityCentral nervous system endothelial cell-polymorphonuclear cell interactions during autoimmune demyelinationEvidence for involvement of ICAM-1 and VCAM-1 in lymphocyte interaction with endothelium in experimental autoimmune encephalomyelitis in the central nervous system in the SJL/J mouse.In vivo expression of inducible nitric oxide synthase in experimentally induced neurologic diseases.Elevated secretion of reactive nitrogen and oxygen intermediates by inflammatory leukocytes in hyperacute experimental autoimmune encephalomyelitis: enhancement by the soluble products of encephalitogenic T cells.The induction of 72-kD gelatinase in T cells upon adhesion to endothelial cells is VCAM-1 dependent.Upregulation and coexpression of adhesion molecules correlate with relapsing autoimmune demyelination in the central nervous system.Differential tumor necrosis factor alpha expression by astrocytes from experimental allergic encephalomyelitis-susceptible and -resistant rat strains.Mechanisms of acquired thymic tolerance in experimental autoimmune encephalomyelitis: thymic dendritic-enriched cells induce specific peripheral T cell unresponsiveness in vivoChronic inflammation caused by lymphotoxin is lymphoid neogenesis.Local delivery of interleukin 4 by retrovirus-transduced T lymphocytes ameliorates experimental autoimmune encephalomyelitis.Antibodies to CD44 and integrin alpha4, but not L-selectin, prevent central nervous system inflammation and experimental encephalomyelitis by blocking secondary leukocyte recruitmentThe activation status of neuroantigen-specific T cells in the target organ determines the clinical outcome of autoimmune encephalomyelitisMonocyte chemotactic protein 1 regulates oral tolerance induction by inhibition of T helper cell 1-related cytokines.Cytosolic phospholipase A2 alpha-deficient mice are resistant to experimental autoimmune encephalomyelitis.Free circulating ICAM-1 in serum and cerebrospinal fluid of HIV-1 infected patients correlate with TNF-alpha and blood-brain barrier damage.Comparative analysis of lesion development and intraspinal inflammation in four strains of mice following spinal contusion injury.Inflammation on the mind: visualizing immunity in the central nervous system.Mice deficient for CCR6 fail to control chronic experimental autoimmune encephalomyelitis.Swift entry of myelin-specific T lymphocytes into the central nervous system in spontaneous autoimmune encephalomyelitis.T-cell apoptosis in inflammatory brain lesions: destruction of T cells does not depend on antigen recognition.Apoptosis of T lymphocytes in experimental autoimmune encephalomyelitis. Evidence for programmed cell death as a mechanism to control inflammation in the brain.
P2860
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P2860
Homing to central nervous system vasculature by antigen-specific lymphocytes. I. Localization of 14C-labeled cells during acute, chronic, and relapsing experimental allergic encephalomyelitis.
description
1990 nî lūn-bûn
@nan
1990年の論文
@ja
1990年学术文章
@wuu
1990年学术文章
@zh
1990年学术文章
@zh-cn
1990年学术文章
@zh-hans
1990年学术文章
@zh-my
1990年学术文章
@zh-sg
1990年學術文章
@yue
1990年學術文章
@zh-hant
name
Homing to central nervous syst ...... al allergic encephalomyelitis.
@en
Homing to central nervous syst ...... al allergic encephalomyelitis.
@nl
type
label
Homing to central nervous syst ...... al allergic encephalomyelitis.
@en
Homing to central nervous syst ...... al allergic encephalomyelitis.
@nl
prefLabel
Homing to central nervous syst ...... al allergic encephalomyelitis.
@en
Homing to central nervous syst ...... al allergic encephalomyelitis.
@nl
P2093
P1476
Homing to central nervous syst ...... al allergic encephalomyelitis.
@en
P2093
P304
P577
1990-08-01T00:00:00Z