title: The Treg/Th17 imbalance in patients with idiopathic dilated cardiomyopathy.
abstract: To assess whether Treg/Th17 balance was broken in patients with idiopathic dilated cardiomyopathy (DCM). We studied 25 patients who were diagnosed as idiopathic DCM (18 men and seven women, mean age 35.6 +/- 5.2) and 25 normal persons (18 men and seven women, mean age 33.8 +/- 4.9). Then, we detected Treg/Th17 functions on different levels including cell frequencies, related cytokine secretion and key transcription factors in patients with idiopathic DCM and controls. The results demonstrated that patients with idiopathic DCM revealed significant increase in peripheral Th17 number, Th17-related cytokines (IL-17, IL-6, IL-23) and transcription factor (RORgammat) levels and obvious decrease in Treg number, Treg-related cytokines (TGF-beta1 and IL-10) and transcription factor (Foxp3) levels when compared to normal persons. Results indicated that Treg/Th17 functional imbalance existed in patients with idiopathic DCM, suggesting a potential role for Treg/Th17 imbalance in the development of idiopathic DCM.
authors.affiliation: Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: S
authors.initials: S
authors.lastname: Wang
authors.forename: H
authors.initials: H
authors.lastname: Zhu
authors.forename: P
authors.initials: P
authors.lastname: Ye
authors.forename: A
authors.initials: A
authors.lastname: Xie
authors.forename: B
authors.initials: B
authors.lastname: Shen
authors.forename: C
authors.initials: C
authors.lastname: Liu
authors.forename: C
authors.initials: C
authors.lastname: Guo
authors.forename: Q
authors.initials: Q
authors.lastname: Fu
authors.forename: K
authors.initials: K
authors.lastname: Zhang
authors.forename: J
authors.initials: J
authors.lastname: Xia
mesh_terms: D000328:Adult; D002311:Cardiomyopathy, Dilated / Q000276:immunology* / Q000378:metabolism; D002469:Cell Separation; D016207:Cytokines / Q000097:blood; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology* / Q000378:metabolism; D008297:Male; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism
chemical_list: D016207:Cytokines; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; C539900:RORC protein, human