Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-4-11
pubmed:abstractText
Traditionally, it is thought that IgE binding to mast cells via the high-affinity receptor (FcepsilonRI) is simply a passive 'sensitization' step prior to activation by receptor aggregation or cross-linking with multivalent antigen or other cross-linking agents. However, in addition to receptor up-regulation, recent studies have shown that monomeric IgE can induce survival and other activation events including increased histamine content, degranulation, leukotriene release, receptor internalization, adhesion, migration and DNA synthesis. Various IgE molecules exhibit a vast spectrum of heterogeneity: the highly cytokinergic (HC) group of IgEs at an extreme end of the spectrum can induce survival and other activation events very efficiently, whereas poorly cytokinergic (PC) IgEs at the other end can do so less efficiently. All the IgEs tested appear to be capable of inducing receptor aggregation with HC IgEs having a higher capacity to do so than PC IgEs. HC IgEs can promote the production and secretion of various cytokines including the one(s) that can sustain survival in an autocrine and paracrine mechanism. Consistent with receptor aggregation induced by monomeric IgE, other means of receptor aggregation, e.g. IgE+antigen and IgE+anti-IgE, can also induce survival and other events in unique ranges of stimulation intensity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1528-2511
pubmed:author
pubmed:issnType
Print
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
100-7; discussion 108-14, 145-51
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
IgE regulation of mast cell survival and function.
pubmed:affiliation
Division of Cell Biology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, California 92121, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural