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Clinical Significance Of CD4~+CD25~+ Regulatory T Cells In The Development Of Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

Posted on:2009-05-02Degree:MasterType:Thesis
Country:ChinaCandidate:Y Y CengFull Text:PDF
GTID:2144360245477148Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective:To investigate the roles of CD4~+CD25~+ T regulatory cells (CD4~+CD25~+Treg),CD4~+T cells and cytokines in the development of Delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Methods: 28 DEACMP patients(16 ineffective,12 remission),10 Acute carbon monoxide poisoning(ACOP) patients and 20 healthy volunteers were enrolled in the study. Peripheral blood samples were obtained in the morning after admission and reobtained before discharge,and serum was collected for IL-10 and TGF-β1 measurement.Flow cytometry was used to quantify CD4~+CD25~+Treg and CD4~+ T cells,and ELISA were carried out to determine the concentrations of IL-10 and TGF-β1.Results:In patients with DEACMP,the rate of CD4~+CD25~+Treg was significantly higher than that in healthy controls(P<0.01 ) and patients with ACOP(P<0.01),but there was no significant difference between ACOP group and control group.In DEACMP group,the rate of CD4~+CD25~+Treg in patients during remission was significantly lower than that in patients at early and ineffective stage(P<0.05).However the rate of CD4~+T cells was comparable in all groups.Compared with healthy controls,TGF-β1 was up-regulated in patients with DEACMP(P<0.05).In addition,TGF-β1 was decreased in patients during remission as compared with patients at early and ineffective stage (P<0.05).The concentration of IL-10 was comparable in all groups.Conclusion: CD4~+CD25~+Treg and TGF-β1 were increased in patients with DEACMP,but decreased in patients during remission,which probably suggested the critical involvement of CD4~+CD25~+Treg and TGF-β1 in the development of DEACMP.
Keywords/Search Tags:CD4~+CD25~+ regulatory T cells, Delayed encephalopathy after acute carbon monoxide poisoning, Acute carbon monoxide poisoning, immunity, TGF-β1, IL-10
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