Identification and verification of differentially expressed key genes in peripheral blood-derived T cells between chronic immune thrombocytopenia patients and healthy controls

Immune thrombocytopenia (ITP), characterized by decreased platelet counts, is a complex immune-mediated disorder with unelucidated pathogenesis. Accumulating evidence shows that T cell-mediated platelet destruction is one crucial process during the progression of ITP. Here, we attempted to identify core genes in peripheral blood-derived T-cells of chronic ITP through the analysis of microarray data (GSE43179) and clinical verification, with the aim to further understand the pathogenesis and progression of ITP. Compared with healthy controls, 97 differentially expressed genes (DEGs), including 63 up-regulated and 34 down-regulated were identified in ITP patients. Functional enrichment analysis showed that the DEGs were mainly enriched in innate immune response, inflammatory response, and IL-17 signaling pathway. Among the DEGs, top 15 hub genes ranked by degree score were identified via protein-protein interaction (PPI) network and were further confirmed by quantitative reverse transcription PCR (qRT-PCR). Among top 15 hub genes, the expression levels of 14 DEGs like TLR4, S100A8, S100A9, and S100A12 were significantly up-regulated, while one DEG IFNG was down-regulated in ITP patients. Noticeably, TLR4 exhibited the highest degree score, and S100A8 had the largest fold change in qRT-PCR analysis. Altogether, our results suggested that the pathogenesis and progression of ITP are related with multiple immune-related pathways, and that TLR4 and S100A8 are likely to play crucial roles.