Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-12-15
pubmed:abstractText
We have previously demonstrated that N-formyl-methionyl-leucyl-phenylalanine (FMLP) induces down-regulation of FcgammaRs on human neutrophils (PMN) modifying different FcgammaR-dependent functions. The aim of this work was to assess the cellular mechanisms by which FMLP exerts this effect on FcgammaRs. The role of the microfilament and cytoskeletal apparatus in this process was evaluated using cytochalasin B (CB), an inhibitor of microfilament functions. The expression of FcgammaRIIIB and FcgammaRII after CB + FMLP treatment was drastically diminished when compared to FMLP-treated cells. Neutrophil degranulation induced by FMLP affect only 22% of the cells in response to FMLP. However, the FcgammaRs of the whole PMN population were reduced, suggesting that secretory products could be responsible for the down-regulation induced by FMLP or FMLP + CB. In fact, supernatants from FMLP-treated PMN also induced FcyRs down-regulation on naive neutrophils. Moreover, supernatants from FMLP + CB-treated PMNs exerted a higher effect. Data obtained from permeabilized PMN show that after FMLP treatment there is an intracellular depletion of both FcgammaRIIIB and FcgammaRII. In addition, the FcgammaR down-regulation is abrogated by phenyl methyl sulfonyl fluoride (PMSF) but not by other protease inhibitors such as pepstatin, thiorphan, phosphoramidon and leupeptin, suggesting a role for serine protease(s) in this process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0165-2478
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
119-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
The down-regulation of FcgammaRII and FcgammaRIIIB by N-formyl-methionyl-leucyl-phenylalanine (FMLP) depends on secretory events in human neutrophils.
pubmed:affiliation
Divisíon Immunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't