免疫系统
SOCS3
免疫学
细胞因子
免疫失调
流式细胞术
发病机制
过敏
车站3
医学
信号转导
淋巴细胞
生物
细胞生物学
作者
Wei Pan,Weihong Tang,Zhongmin Wang,Yunyun Deng,Shan Ye
标识
DOI:10.1177/09287329251360089
摘要
BackgroundCow's milk protein allergy (CMPA) is a common food allergy in children, affecting growth, development, and quality of life. The pathogenesis involves immune dysregulation, particularly CD4+ T lymphocyte subsets, which play a key role in immune responses. The JAK2-STAT3 signaling pathway is critical for immune cell regulation, but its role in CMPA-associated immune changes remains unclear.MethodsA total of 103 CMPA patients and 100 healthy controls were enrolled. Peripheral blood samples were collected from patients before and after a 3-month CMPA avoidance diet. Flow cytometry, ELISA, western blotting, and qRT-PCR were used to analyze CD4+ T cell subsets (Th1, Th2, Th17), cytokine levels, and JAK2-STAT3 pathway activity.ResultsCMPA patients exhibited increased Th2 and Th17 proportions and reduced Th1 cells compared to controls. JAK2 and STAT3 phosphorylation levels were elevated, while SOCS1/SOCS3 expression was downregulated. After dietary avoidance, Th2 and Th17 proportions decreased, Th1 increased, and JAK2-STAT3 activation normalized. Pearson correlation analysis revealed positive associations between JAK2-STAT3 activation and Th2/Th17 proportions and a negative correlation with Th1.ConclusionsThe JAK2-STAT3 signaling pathway is abnormally activated in CMPA and correlates with CD4+ T lymphocyte subset imbalances. Targeting this pathway may offer therapeutic potential for CMPA management.
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