Increased circulating T‑helper 22 cells in patients with dilated cardiomyopathy.

Recently, the newly determined interleukin (IL)‑22‑producing T-helper (Th) 22 cell has been implicated to be involved in the pathogenesis of autoimmune diseases. However, its role in the pathogenesis of dilated cardiomyopathy (DCM) has yet to be elucidated. A total of 30 patients with DCM and 30 healthy controls were enrolled in the present study. The levels of Th22, Th17 and Th1 cells in the peripheral blood were analyzed by flow cytometry. Levels of plasma IL‑22 and autoantibody adenine nucleotide translocator (ANT) were assessed using the ELISA. The key transcription factor of Th22, aryl hydrocarbon receptor (AHR), was assessed using quantitative polymerase chain reaction. Additionally, clinical data on the brain natriuretic peptide (BNP), C‑reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were collected. In comparison with those in the control group, significantly elevated levels of Th22, Th17 and Th1 cells were detected in patients with DCM (all P<0.01). Similarly, elevated mRNA levels of peripheral AHR were detected in patients with DCM. The percentage of Th22 cells was higher in ANT‑positive compared with ANT‑negative patients with DCM. The levels of BNP and CRP, but not ESR, showed a significant positive correlation with those of Th22 cells. With regard to the concentrations of plasma IL‑22, no statistical difference was found between patients with DCM and the healthy controls, nor did it demonstrate a statistical correlation with the percentage of Th22 cells. In conclusion, the present study showed that patients with DCM, particularly those of the ANT autoantibody positive subjects, exhibit elevated levels of peripheral Th22 cells, indicating that a Th22 immune response may be implicated in the pathogenesis of DCM.