Linked Life Data

1380045

Source:http://linkedlifedata.com/resource/pubmed/id/1380045

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1992-9-14
pubmed:abstractText
To determine whether there is predominance of T cells expressing a particular TCR V beta chain in the inflammatory lesions of an autoimmune disease model, TCR expression was analyzed in central nervous system (CNS) tissues of mice with experimental allergic encephalomyelitis (EAE). Acute EAE was induced in SJL/J mice either by sensitization with a synthetic peptide corresponding to myelin proteolipid protein residues 139-151 or by adoptive transfer of myelin proteolipid protein peptide 139-151-specific encephalitogenic T cell clones. Mice were killed when they showed clinical signs of EAE or by 40 days after sensitization or T cell transfer. Cryostat CNS and lymphoid tissue sections were immunostained with a panel of mAb to T cell markers and proportions of stained cells were counted in inflammatory foci. In mice with both actively induced and adoptively transferred EAE, infiltrates consisted of many CD3+, TCR alpha beta+, and CD4+ cells, fewer CD8+ cells, and small numbers of TCR gamma delta+ cells. Approximately 30% of CD45+ leukocytes in the inflammatory foci were T cells. Cells expressing TCR V beta 2, 3, 4, 6, 7 and 14 were detected in the infiltrates, whereas TCR V beta 8 and 11, which that are deleted in SJL mice, were absent. When EAE was induced by transfer of T cell clones that use either V beta 2, 6, 10, or 17, there was also a heterogeneous accumulation of T cells in the lesions. Similar proportions of TCR V beta+ and gamma delta+ cells were detected in EAE lesions and in the spleens of the mice. Thus, at the time that clinical signs are present in acute EAE, peripherally derived, heterogeneous TCR V beta+ cells are found in CNS lesions, even when the immune response is initiated to a short peptide Ag or by a T cell clone using a single TCR V beta.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
149
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1444-51
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1380045-Amino Acid Sequence, pubmed-meshheading:1380045-Animals, pubmed-meshheading:1380045-Antigens, CD3, pubmed-meshheading:1380045-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1380045-Brain, pubmed-meshheading:1380045-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:1380045-Female, pubmed-meshheading:1380045-Immunity, Cellular, pubmed-meshheading:1380045-Immunization, Passive, pubmed-meshheading:1380045-Immunohistochemistry, pubmed-meshheading:1380045-Mice, pubmed-meshheading:1380045-Mice, Inbred Strains, pubmed-meshheading:1380045-Molecular Sequence Data, pubmed-meshheading:1380045-Myelin Proteins, pubmed-meshheading:1380045-Myelin Proteolipid Protein, pubmed-meshheading:1380045-Peptides, pubmed-meshheading:1380045-Receptors, Antigen, T-Cell, pubmed-meshheading:1380045-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:1380045-Receptors, Antigen, T-Cell, gamma-delta, pubmed-meshheading:1380045-Spleen, pubmed-meshheading:1380045-T-Lymphocytes
pubmed:year
1992
pubmed:articleTitle
The immunopathology of acute experimental allergic encephalomyelitis induced with myelin proteolipid protein. T cell receptors in inflammatory lesions.
pubmed:affiliation
Department of Pathology, Massachusetts General Hospital, Boston 02114.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't