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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0017262,
umls-concept:C0023473,
umls-concept:C0041904,
umls-concept:C0086418,
umls-concept:C0162388,
umls-concept:C0162493,
umls-concept:C0185117,
umls-concept:C0442805,
umls-concept:C1423033,
umls-concept:C1514559,
umls-concept:C1539477,
umls-concept:C2709199,
umls-concept:C2911684
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pubmed:issue |
14
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pubmed:dateCreated |
2011-4-4
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pubmed:abstractText |
IL-32 was recently identified as a proinflammatory cytokine that is induced by IL-18 in natural killer (NK) cells and is highly correlated with inflammatory disorders. However, the relationship between IL-32 and tumor progression is still unknown. In this study, we investigated whether overexpression of IL-32 affects susceptibility of chronic myeloid leukemia (CML) cells to NK cells. Interestingly, IL-32?-overexpressing CML cell lines, K562, Kcl22, and BV173, showed higher NK cell-mediated killing. Flow cytometry analysis revealed that overexpression of IL-32? induced increased expression of Fas and UL16-binding protein 2 (ULBP2) in CML cells. The direct relationship between overexpression of surface molecules by IL-32? and increased NK cell-mediated killing was confirmed by Fas or ULBP2 siRNA transfection. IL-32?-induced Fas and ULBP2 expression are regulated p38 MAPK. In addition, the transcription factor Ets1 plays a key role in ULBP2 specific expression by IL-32? overexpression in ULBP family members. Taken together, these data show that IL-32? stimulates Fas and ULBP2 expression via activation of p38 MAPK, which increases NK susceptibility of CML cells. Enhanced NK cell susceptibility of CML cells by IL-32? overexpression may improve the efficiency of NK cell-based immunotherapy.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/ETS1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/FAS protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/GPI-Linked Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/IL32 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Protein c-ets-1,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/ULBP2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1083-351X
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pubmed:author |
pubmed-author:BangSa IkSI,
pubmed-author:CheonSoyoungS,
pubmed-author:ChoByung JooBJ,
pubmed-author:ChoDaehoD,
pubmed-author:JeongSeung HwanSH,
pubmed-author:KimTaesungT,
pubmed-author:LeeHyong JooHJ,
pubmed-author:LeeJi HyungJH,
pubmed-author:LeeKi WoongKW,
pubmed-author:LeeWang JaeWJ,
pubmed-author:MinHyeyoungH,
pubmed-author:ParkHyunjeongH,
pubmed-author:ParkSunyoungS,
pubmed-author:YoonDo-YoungDY,
pubmed-author:YoonSung-SooSS
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pubmed:issnType |
Electronic
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pubmed:day |
8
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
12049-55
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pubmed:meshHeading |
pubmed-meshheading:21321117-Antigens, CD95,
pubmed-meshheading:21321117-Blotting, Western,
pubmed-meshheading:21321117-Cell Line,
pubmed-meshheading:21321117-Cell Line, Tumor,
pubmed-meshheading:21321117-Flow Cytometry,
pubmed-meshheading:21321117-GPI-Linked Proteins,
pubmed-meshheading:21321117-Humans,
pubmed-meshheading:21321117-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:21321117-Interleukins,
pubmed-meshheading:21321117-Killer Cells, Natural,
pubmed-meshheading:21321117-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:21321117-Proto-Oncogene Protein c-ets-1,
pubmed-meshheading:21321117-RNA, Small Interfering,
pubmed-meshheading:21321117-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21321117-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2011
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pubmed:articleTitle |
Overexpression of IL-32alpha increases natural killer cell-mediated killing through up-regulation of Fas and UL16-binding protein 2 (ULBP2) expression in human chronic myeloid leukemia cells.
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pubmed:affiliation |
Department of Life Science, Sookmyung Women's University, and Konkuk University Hospital, Seoul 140-742, Republic of Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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