关贸总协定3
状态4
FOXP3型
免疫学
细胞因子
转录因子
CD19
RAR相关孤儿受体γ
医学
生物
抗体
免疫系统
车站3
信号转导
斯达
基因
细胞生物学
遗传学
作者
Serkan Küççüktürk,Mehmet Ali Karaselek,Tuğçe Duran,İsmail Reisli
出处
期刊:Apmis
[Wiley]
日期:2023-12-14
卷期号:132 (2): 122-129
被引量:2
摘要
CD19 deficiency is a rare, predominantly antibody deficiency, and there are few studies showing that it can be seen in autoimmune diseases. The aim of study was evaluated to transcription factor and cytokine expressions of helper T (Th)‐cell subsets in CD19 deficiency and the possible mechanism role of this factor expression in autoimmune disease. Transcription factor and cytokine expressions of Th1, Th2, Th17, and regulatory T (Treg) cells were investigated by real‐time polymerase chain reaction (qPCR) method. In the study, in the patient/control comparison, transcription factor and cytokine expressions of Th1 (T‐bet, STAT1, and STAT4) were found to be significantly downregulated, but IFN‐γ was significantly upregulated in patients. Th2 factor GATA3, STAT6, IL‐4, and IL‐5 were significantly downregulated. For Th17, RORγt was downregulated while IL‐22 was upregulated. In the heterozygous/control comparison, there was no significant change in gene expressions other than IL‐5. T‐bet, STAT1, GATA3, IL‐4, RORγt, FoxP3, and TGF‐β were significantly downregulated in the patient/heterozygous comparison. It was revealed for the first time that the expression of the transcription factors and cytokines in CD19 deficiency. These findings might be showing the predominance of Th1 factors and suppressed Treg factors which could be related with autoimmunity in CD19 deficiency.
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