Source:http://linkedlifedata.com/resource/pubmed/id/19597336
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
16
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pubmed:dateCreated |
2009-8-17
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pubmed:abstractText |
Regulatory T cells (Tregs) in peripheral blood and tumor infiltrating lymphocytes (TILs) play crucial roles in suppressing anti-tumor immune responses in cancer patients, and correlate with clinical outcomes. We identified an important subpopulation, CD13+CD4+CD25hiTreg cells, among CD4+CD25hiTreg cells in the peripheral blood of non-small cell lung cancer (NSCLC) patients. Peripheral blood mononuclear cells (PBMCs) were isolated from patients with NSCLC (n = 72) or from healthy donors (n = 30). Flow cytometric analyses were performed to study the expression of cell-surface or intracellular markers on the CD4+CD25hiTreg cells. The immune suppressive function of CD13+CD4+CD25hiTreg cells was evaluated by co-culturing with CD4+CD25-T cells that were activated by PHA. Our data showed that, compared with CD4+CD25(Low/-)T cells, CD13 expression was enriched on CD4+CD25hiTreg cells. The CD13+CD4+CD25hiTreg cells also expressed higher levels of Foxp3, CTLA-4, membrane-bound transforming growth factor beta1 (mTGFbeta1) and B7-H1, and are more suppressive to CD25 expression and proliferation of CD4+CD25-T cells. Additionally, we showed that the expression of Foxp3, CTLA-4, B7-H1, mTGFbeta1 and the secretion of TGFbeta1 and IL-10 on CD13+CD4+CD25hiTreg cells was significantly suppressed by anti-CD13 mAb (WM15), and the ability of these cells to suppress CD25 expression and proliferation of CD4+CD25-T cells was inhibited by WM15 as well. Interestingly, the percentage of CD13+CD4+CD25hiTreg cells among the CD4+CD25hiTreg population increased significantly and correlated with pathological stage in NSCLC: healthy donor (9.84% +/- 2.23%) <stage I (21.64% +/- 2.78%) <stage II (31.86% +/- 3.01%) <stage III (45.64% +/- 6.12%) <stage IV (58.78% +/- 12.89%). Moreover, the percentage of CD13+CD4+CD25hiTreg cells decreased dramatically after surgical removal of tumors. CD13 is a new surface molecule for identifying a CD4+CD25hiTreg cell subpopulation with higher suppressive ability. The percentage of CD13+CD4+CD25hiTreg cells among the CD4+CD25hiTreg cell population correlated with the pathological stage in NSCLC and tumor burden. CD13 represents a potential target to suppress Treg cells in anti-tumor therapy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1551-4005
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pubmed:author |
pubmed-author:GeYanY,
pubmed-author:HuangXinenX,
pubmed-author:JohnsonDaniel EDE,
pubmed-author:JuSongguangS,
pubmed-author:JuSongwenS,
pubmed-author:LiJuanJ,
pubmed-author:LiuLinxiangL,
pubmed-author:QiuHongxiaH,
pubmed-author:ShuYongqianY,
pubmed-author:ZenTT,
pubmed-author:ZhangYuY,
pubmed-author:ZhouXiaoyueX,
pubmed-author:ZhuBiqinB
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2578-85
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pubmed:meshHeading |
pubmed-meshheading:19597336-Adult,
pubmed-meshheading:19597336-Aged,
pubmed-meshheading:19597336-Aged, 80 and over,
pubmed-meshheading:19597336-Antigens, CD13,
pubmed-meshheading:19597336-Antigens, CD4,
pubmed-meshheading:19597336-Carcinoma, Non-Small-Cell Lung,
pubmed-meshheading:19597336-Cell Proliferation,
pubmed-meshheading:19597336-Cells, Cultured,
pubmed-meshheading:19597336-Female,
pubmed-meshheading:19597336-Flow Cytometry,
pubmed-meshheading:19597336-Humans,
pubmed-meshheading:19597336-Interleukin-2 Receptor alpha Subunit,
pubmed-meshheading:19597336-Male,
pubmed-meshheading:19597336-Middle Aged,
pubmed-meshheading:19597336-T-Lymphocytes, Regulatory
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pubmed:year |
2009
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pubmed:articleTitle |
CD13+CD4+CD25hi regulatory T cells exhibit higher suppressive function and increase with tumor stage in non-small cell lung cancer patients.
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pubmed:affiliation |
Cancer Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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