CXCL10/IFN-γ-induced protein 10 (IP-10) and its corresponding receptor CXCR3 have long been considered to be involved in the pathophysiology of type 1 T (Th1) cell-orientated autoimmune diseases. However, the exact role of CXCL10 in the pathogenesis of aplastic anaemia (AA) has not been thoroughly studied. The aim of our study was to evaluate the plasma level of CXCL10 and its effects on CD4+ T cell differentiation in AA. In our study, we found that an elevated plasma level of CXCL10 was negatively correlated with platelet, absolute neutrophil and reticulocyte counts, while it was positively correlated with the proportion of lymphocytes in white blood cells in AA patients. To confirm the pro-inflammatory effects of CXCL10 in AA, we isolated CD4+ T cells and evaluated the function of CXCL10 in CD4+ T cell differentiation. In vitro stimulation experiments further revealed the pro-inflammatory role of CXCL10 in AA, partially by promoting the secretion of interferon (IFN)-γ and IL-17. In addition, CXCL10 significantly skewed CD4+ T cell differentiation to Th1 cells and T helper 17 (Th17) cells in AA patients, while it inhibited the differentiation of type 2 T (Th2) cells only in controls. The mRNA expression of transcription factors representative of T cell differentiation was detected by RT-PCR. Consistently, our results showed that after CXCL10 treatment, the expression of T-bet and RORγt was significantly enhanced, while the expression of GATA3 was inhibited. In conclusion, our results indicated that CXCL10, a pro-inflammatory chemokine, might be involved in the abnormal immune response in AA.