Linked Life Data

1362438

Source:http://linkedlifedata.com/resource/pubmed/id/1362438

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1993-2-12
pubmed:abstractText
Prominent inflammation in the demyelinative lesion of adreno-leukodystrophy (ALD) has suggested an immune-mediated pathogenetic component. Commercially available antibodies to T cells, B cells, macrophages, class I and II molecules, complement, IgG, IgM, IgA, interleukin-1 (IL-1), intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF) were applied to paraffin sections of formaldehyde-fixed postmortem samples. Twenty-five primary demyelinative lesions from five juvenile ALD, three adult ALD, and three adrenomyeloneuropathic patients were evaluated with appropriate positive and negative controls. Macrophages and astrocytes were the predominant cells detected at the active edge; T lymphocytes, including T4 and CD45R subsets, were nearly as numerous but usually located around vessels within the lesion. B cells and plasma cells, usually containing IgG, were uncommon. The expression of class II molecules, restricted to one adult, was problematic; class I expression was increased in microvascular and other cells. Degraded myelin was labeled with antibodies to C3d and IL-1; IL-1 and ICAM-1 immunoreactivity was seen on microvessels and astrocytes. Tumor necrosis factor-alpha immunoreactivity was detected in macrophages, but more prominently in astrocytes. These data support a natural immune response in the demyelinative lesion of ALD, consisting predominantly of reactive astrocytes, macrophages, T cells and cytokines. A two-stage pathogenetic theory is discussed. The postulated roles of TNF and reactive astrocytes, in concert with a fundamental myelinolytic biochemical defect, suggest a different pathogenetic mechanism and raise novel therapeutic possibilities.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-3069
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
630-43
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1362438-Adrenoleukodystrophy, pubmed-meshheading:1362438-Adult, pubmed-meshheading:1362438-B-Lymphocytes, pubmed-meshheading:1362438-Brain, pubmed-meshheading:1362438-Cell Adhesion, pubmed-meshheading:1362438-Cell Adhesion Molecules, pubmed-meshheading:1362438-Child, pubmed-meshheading:1362438-Complement System Proteins, pubmed-meshheading:1362438-Demyelinating Diseases, pubmed-meshheading:1362438-HLA-D Antigens, pubmed-meshheading:1362438-Histocompatibility Antigens Class I, pubmed-meshheading:1362438-Humans, pubmed-meshheading:1362438-Immunoglobulin A, pubmed-meshheading:1362438-Immunoglobulin M, pubmed-meshheading:1362438-Intercellular Adhesion Molecule-1, pubmed-meshheading:1362438-Macrophages, pubmed-meshheading:1362438-Multiple Sclerosis, pubmed-meshheading:1362438-Retrospective Studies, pubmed-meshheading:1362438-T-Lymphocytes, pubmed-meshheading:1362438-Tumor Necrosis Factor-alpha
pubmed:year
1992
pubmed:articleTitle
The inflammatory myelinopathy of adreno-leukodystrophy: cells, effector molecules, and pathogenetic implications.
pubmed:affiliation
Department of Pathology, Columbia-Presbyterian Medical Center, New York, New York.
pubmed:publicationType
Journal Article, Comparative Study