Literature DB >> 17219964

CD4+CD25high regulatory cells in peripheral blood of NSCLC patients.

Li Liu1, Junxia Yao, Qian Ding, Shiang Huang.   

Abstract

The proportion and changes of CD4+CD25high regulatory T cells (Trs) in peripheral blood of non-small cell lung cancer (NSCLC) patients were analyzed and their clinical significance explored. The peripheral blood was collected from 61 patients with NSCLC and 15 healthy controls. By using monoclonal antibodies, the blood samples were evaluated with the flow cytometry for lymphocyte subsets (CD3+, CD4+ and CD8+) and CD4+CD25high Tr cells. The results showed that the proportion of CD4+CD25high Tr cells in NSCLC group was significantly higher than in control group [(4.36 +/-2.07) % vs (2.04+/-1.03) %, P<0.01]. The proportion of CD4+CD25 high Tr cells in late stage was higher than that in early stage [stages I +II (2.26+/-0.6) %; stage III (3.28+/-1.38) %; stage IV (6.06 +/-4.08) %] (P<0.05). Kaplan-Meier survival analysis revealed that the prognosis of the patients who had higher proportion of CD4+CD25high Tr cells in peripheral blood was worse (P=0.0026). In conclusion, the relative increase in CD4+CD25high Tr cells in peripheral blood may be related to immunosuppression and tumor progression in patients with NSCLC. This finding suggests that CD4+CD25+high Tr cells in peripheral blood of NSCLC may be positive for prognosis analysis. The use of depletion of the CD4+CD25high Tr cell therapy to treat NSCLC patients may be an effective strategy.

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Year:  2006        PMID: 17219964     DOI: 10.1007/s11596-006-0516-5

Source DB:  PubMed          Journal:  J Huazhong Univ Sci Technolog Med Sci        ISSN: 1672-0733


  11 in total

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4.  Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases.

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Authors:  E M Shevach
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3.  CD4+CD25hiCD127low regulatory T cells are increased in oral squamous cell carcinoma patients.

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6.  Elevated regulatory T cells, surface and intracellular CTLA-4 expression and interleukin-17 in the lung cancer microenvironment in humans.

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