Relationship between the severity of iron overload in peripheral blood CD4+ T cells and the key transcription factors of RORrt, IRF8, STAT3 for cell proliferation and differentiation in elderly patients with myelodysplastic syndrome

Abstract

Objective To investigate the effects RORrt(RORrt), IRF8(IRF8)and STAT3(STAT3)in peripheral blood CD4+ T cells on the cell proliferation and differentiation in elderly patients with iron-overload myelodysplastic syndrome(MDS). Methods A prospective case-control study was conducted.Twenty-two elderly hospitalized patients(12 males and 10 females)aged 60-78 years with iron-overload MDS from Jan.2017 to Dec.2018 were enrolled and considered as the observation group.Twenty MDS patients without iron overload hospitalized in the same period were selected as the non-iron overload group, and 26 healthy elderly people were considered as the healthy control group.Peripheral blood monocytes(PBM)were prepared and resident CD4+ T cells were sorted by flow cytometry.The mRNA and protein expression levels of transcription factors of RORrt, p-STAT3 and IRF8 were detected by quantitative real time polymerase chain reaction(qRT-PCR)and Western blotting. Results In peripheral blood CD4+ T cells, the mRNA expression level of RORrt and p-STAT3 were higher and that of IRF8 was lower in the iron-overload group than in the non-iron overload group and the healthy control group(42.634±18.613 vs.21.289±15.158 and 22.520±9.896; 29.710±9.689 vs.12.355±4.681 and 9.818±3.845; 19.293±8.258 vs.23.785±12.498 and 69.619±23.768, P<0.01). In peripheral blood CD4+ T cells, the protein expression level of RORrt and p-STAT3 was higher, and that of IRF8 was lower in the iron overload group than in the non-iron overload group and healthy control group(P<0.01). Conclusions The abnormalities of the mRNA and protein expression levels of transcription factors of RORrt, IRF8 and p-STAT3 in CD4+ T cells play a fundamental role in the pathogenesis of iron overload MDS in elderly patients. Key words: Myelodysplastic syndrome; Antigens, CD4; Interferon regulatory factors