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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-12-6
pubmed:abstractText
Fcgamma receptor IIIa (Fc?RIIIa) polymorphisms is considered to influence clinical response to therapeutic monoclonal antibody (McAb) in cancer, most people believe it can affect McAb binding, and McAb-dependent NK cell-mediated cytotoxicity. This study was purposed to determine the difference of antibody-dependent cell-mediated cytotoxicity (ADCC) effects mediated by different Fc?RIIIa NK cells. The Fc?RIIIa genotypes were detected by nest-PCR, the target cells (Raji cells) were stained with 5- (and 6-) carboxyfluorescein diacetate succinimidyl ester (CFSE), cultured with effector cells with different Fc?RIIIa genotypes, and finally stained with propidium iodide (PI); the CD20 expression of Raji cells were tested by flow cytometry and cytotoxic index was calculated as well. The results indicated that the ADCC cytotoxic indexes of NK cells with Fc?RIIIa-158V/V and Fc?RIIIa-158V/F were 69.05±2.38% and 39.63±3.86% respectively, as compared with NK cells with Fc?RIIIa158 V/V, ADCC effect of NK cells with Fc?RIIIa-158 on Raji cells was obviously weakened with significant difference (p<0.05). It is concluded that Fc?RIIIa polymorphism can influence ADCC activity of NK cells, ADCC activity of NK cells with Fc?RIIIa-158V/V is higher than that of NK cells with Fc?RIIIa-158V/F.
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1009-2137
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1269-74
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
[Influence of Fc?RIIIa polymorphism on rituximab-dependent NK cell-mediated cytotoxicity to Raji cells].
pubmed:affiliation
Department of Pediatrics, Sun Yet-Sen Memorial Hospital, Sun Yet-Sen University, Guangzhou 510120, Guangdong Province, China.
pubmed:publicationType
Journal Article, English Abstract, Research Support, Non-U.S. Gov't