T helper (Th) 17 cells are a subset of Th cells expressing interleukin‐ (IL‐) 17 and initiating an inflammatory response in autoimmune diseases. Graft‐versus‐host disease (GVHD) is an immune inflammatory disease caused by interactions between the adaptive immunity of donor and recipient. The Th17 lineage exhibits proinflammatory activity and is believed to be a central player in GVHD. IL‐1 performs a key function in immune responses and induces development of Th17 cells. Here, we show that blockade of IL‐1 signaling suppresses Th17 cell differentiation and alleviates GVHD severity. We hypothesized that the IL‐1 receptor antagonist (IL‐1Ra) would suppress Th17 cell differentiation in vitro via inhibition of glycolysis‐related genes. Blockade of IL‐1 using IL‐1Ra downregulated Th17 cell differentiation, an alloreactive T cell response, and expression of genes of the glycolysis pathway. Severity of GVHD was reduced in mice with a transplant of IL‐Ra‐treated cells, in comparison with control mice. To clarify the mechanisms via which IL‐1Ra exerts the therapeutic effect, we demonstrated in vivo that IL‐1Ra decreased the proportion of Th17 cells, increased the proportion of FoxP3‐expressing T regulatory (T_reg) cells, and inhibited expression of glycolysis‐related genes and suppressed Th17 cell development and B‐cell activation. These results suggest that blockade of IL‐1 signaling ameliorates GVHD via suppression of excessive T cell‐related inflammation.