Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-4-2
pubmed:abstractText
Signals through HLA-DR molecules contribute to optimal activation of antigen-presenting cells (APC) during T cell/APC interactions participating in the generation of productive interactions, and to the induction of APC death, which has been postulated to play a role in the termination of the immune response. To understand how these molecules accommodate both cellular responses, we studied the not yet well-defined signaling events and the biochemical requirements for HLA-DR-mediated death. We demonstrate that in B cells the HLA-DR-activated protein kinase C (PKC) beta is required for HLA-DR-mediated death whereas the HLA-DR-activated Src family of PTK is redundant. In contrast to HLA-DR-mediated activation of Src kinase Lyn, the aggregation of HLA-DR molecules in lipid rafts is not required for HLA-DR-mediated PKC beta activation nor for the induction of cell death. Indeed, the bulk of HLA-DR-activated PKC beta reside outside rafts. This is the first report showing that HLA-DR-induced PKC beta activation is essential for the induction of B cell death via HLA-DR, and that these HLA-DR-mediated events do not require the integrity of rafts.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
928-38
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Signaling through HLA-DR induces PKC beta-dependent B cell death outside rafts.
pubmed:affiliation
Centre de Recherche en Rhumatologie et Immunologie, CHUL, Université Laval, Québec, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't