International journal of clinical and experimental pathology · 2014
Different levels of circulating Th22 cell and its related molecules in Graves' disease and Hashimoto's thyroiditis.
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Song Rong-Hua, Yu Zhi-Yun, Qin Qiu, Wang Xuan, Muhali Fatuma-Said, Shi Liang-Feng, Jiang Wen-Juan, Xiao Ling, Li Dan-Feng, Zhang Jin-An
Аннотация
PURPOSE: The aim of this study was to make a comparative analysis of the possible different expression of Th22 cells in two subtypes of autoimmune thyroid diseases (AITDs), i.e., Graves' disease (GD) and Hashimoto's thyroiditis (HT).
METHODS: We recruited 61 AITDs patients (31 GD and 30 HT) and 22 controls. Serum level of IL-22 was measured by enzyme linked immunosorbent assay (ELISA). The proportion of Th22 cells in peripheral blood mononuclear cells (PBMCs) was analyzed by flow cytometry. The messenger RNA (mRNA) expressions of IL-22, its receptors (IL10R2, IL22R1) and key transcription factor (aryl hydrocarbon receptor, AHR) in PBMCs were assayed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Several cytokines of the cultured PBMCs were also measured under IL-22 stimulation.
RESULTS: The proportion of Th22 cells, serum IL22 level and IL-22 mRNA expression were significantly higher in patients with GD than in healthy controls. Additionally, AHR increased in GD patients compared to healthy controls. However, the elevation of Th22 cells and their relative cytokines was not found in patients with HT. Consistent with specific mRNAs expression of cultured PBMCs, IL-4 increment in supernatant was much higher in GD group than in control group, while IFN-γ levels were decreased under IL-22 stimulation.
CONCLUSION: Th22 cells may participate in the pathogenesis of AITDs as a proinflammatory factor, especially in GD, through expressing and secreting IL-22.
METHODS: We recruited 61 AITDs patients (31 GD and 30 HT) and 22 controls. Serum level of IL-22 was measured by enzyme linked immunosorbent assay (ELISA). The proportion of Th22 cells in peripheral blood mononuclear cells (PBMCs) was analyzed by flow cytometry. The messenger RNA (mRNA) expressions of IL-22, its receptors (IL10R2, IL22R1) and key transcription factor (aryl hydrocarbon receptor, AHR) in PBMCs were assayed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Several cytokines of the cultured PBMCs were also measured under IL-22 stimulation.
RESULTS: The proportion of Th22 cells, serum IL22 level and IL-22 mRNA expression were significantly higher in patients with GD than in healthy controls. Additionally, AHR increased in GD patients compared to healthy controls. However, the elevation of Th22 cells and their relative cytokines was not found in patients with HT. Consistent with specific mRNAs expression of cultured PBMCs, IL-4 increment in supernatant was much higher in GD group than in control group, while IFN-γ levels were decreased under IL-22 stimulation.
CONCLUSION: Th22 cells may participate in the pathogenesis of AITDs as a proinflammatory factor, especially in GD, through expressing and secreting IL-22.