Evaluation of transcription factors and cytokine expressions of T-cell subsets in CD19 deficiency and their possible relationship with autoimmune disease

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-gamma was significantly upregulated in patients. Th2 factor GATA3, STAT6, IL-4, and IL-5 were significantly downregulated. For Th17, ROR gamma t 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, ROR gamma t, FoxP3, and TGF-beta 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.

Automated summary

CD19 deficiency is associated with altered expression of transcription factors and cytokines in T-cell subsets, particularly with downregulation of Th1 factors and upregulation of IFN-gamma. This suggests a potential role of CD19 deficiency in autoimmune diseases.