Increase in different peripheral effector T subsets in acute and chronic gout

Gout (GT) belongs to a group of diseases caused by a purine metabolic disorder. GT is an inflammatory disease caused by the local deposition of uric acid in joints or adjacent tissues. The mechanism of GT is not fully explained, especially the involvement of an immune system. The objective of this study was to investigate the change in peripheral CD4⁺T subsets in acute and chronic GT patients.

A total of 205 patients with acute and chronic GT and 87 healthy controls (HCs) were enrolled. The medical history improvement, clinical indicators, immune function, and peripheral CD4⁺T-lymphocyte detected by modified flow cytometry were collected in all subjects.

Compared with healthy controls, acute and chronic GT patients remarkably increased the absolute counts of T helper type 1 (Th1) cells (P < 0.05) and decreased the absolute number of Treg cells without significant difference (P > 0.05). In addition, the absolute number and percentage of Th1 cells and Th1/T helper type 2 (Th2) ratio increased significantly, and the ratio of Th2 cells decreased in patients with chronic GT compared to patients with acute GT (P < 0.05). The results of Spearman correlation analysis showed a notably negative correlation between the level of CRP and the absolute counts of peripheral Th1 and Th17 cells in patients with GT, while the levels of CD4⁺T sunsets had no significant correlation with ESR and uric acid. The course of the disease, the absolute number of Th1 cells, the percentage of Th1 cells and the ratio of Th1/Th2 cells were significantly associated with the progression of the disease, and the course of the disease was an independent risk factor for patients with chronic GT.

The balance of Th1 and Th2 were involved throughout the whole stages of GT, Th17 cells then become involved in the disease process as the disease progresses.