Linked Life Data

7716542

Source:http://linkedlifedata.com/resource/pubmed/id/7716542

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5209
pubmed:dateCreated
1995-5-18
pubmed:abstractText
Bacterial superantigens bind with high affinity to major histocompatibility complex (MHC) class II antigens on antigen-presenting cells and with T cell antigen receptor (TCR) beta chains on T lymphocytes, which results in the T cell activation responsible for toxic shock syndrome and food poisoning. Many cytotoxic T lymphocyte (CTL) clones were shown to have receptors for human leukocyte antigen (HLA) class I molecules that inhibited superantigen-induced cytotoxicity against appropriate class I-bearing target cells. One type of inhibitory receptor, NKB1, was present on CD4+ and CD8+TCR alpha beta+ CTL clones and blocked the killing of staphylococcal enterotoxin B (SEB)-coated targets bearing certain polymorphic HLA-B molecules. Expression of HLA-A, -B, and -C molecules on the SEB-coated targets also protected against cytolysis mediated by many NKB1-negative T cell clones, suggesting the presence of additional inhibitory MHC class I receptors. These HLA class I receptors may limit tissue destruction and possibly autoimmunity caused by activated T lymphocytes.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
403-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Superantigen-dependent, cell-mediated cytotoxicity inhibited by MHC class I receptors on T lymphocytes.
pubmed:affiliation
Department of Human Immunology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't