Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1989-5-2
pubmed:abstractText
Fresh-frozen autopsy material containing active inflammatory lesions from 9 different patients with multiple sclerosis (MS) was analyzed by immunocytochemistry using a panel of monoclonal antibodies, and a dual-label immunocytochemical method was developed which permitted the simultaneous detection of two different surface markers on a single cell. We now report the following. (1) The predominant T-cell phenotype within MS lesions is CD2,3,8. This phenotype marks the suppressor-cytotoxic subset. (2) These cells do not express the natural killer cell marker NKH-1, which is present on a subset of CD8-positive cells in peripheral blood. (3) The infiltrating cell expresses class I (HLA A, B, C), but not class II (DR and DQ), major histocompatibility complex (MHC) molecules. (4) Other T-cell surface molecules, including the activation antigens interleukin-2 receptor, Ta1, and T11-3, as well as the marker 2H4, are largely not expressed. (5) Endothelial cells express both class I and class II MHC molecules and the 4B4 molecule in both MS and control tissue. (6) Astrocytes within the vicinity of MS lesions are predominantly class II MHC-negative. These results demonstrate that the T-cell infiltrate present in MS tissue on autopsy has a restricted phenotypic profile, but they also raise the possibility that, within this population, few activated effector cells are present.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0364-5134
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
523-31
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Dual-label immunocytochemistry of the active multiple sclerosis lesion: major histocompatibility complex and activation antigens.
pubmed:affiliation
Neuroimmunology Unit, Massachusetts General Hospital, Boston 02114.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't