The current study explored our hypothesis that IFN‐γ‐producing human T cells inhibit human osteoclast formation. Activated T cells derived from human PBMC were divided into IFN‐γ‐producing T cells (IFN‐γ⁺ T cells) and IFN‐γ‐non‐producing T cells (IFN‐γ^– T cells). IFN‐γ⁺ T cells were cultured with human monocytes in the presence of macrophage‐CSF alone. The concentration of soluble receptor activator of NF‐κB ligand (RANKL) and IFN‐γ, and the amount of membrane type RANKL expressed on T cells, were measured by ELISA. In the patients with early rheumatoid arthritis (RA) treated with non‐steroidal anti‐inflammatory drugs alone, CD4⁺ T cells expressing both IFN‐γ and RANKL were detected by flow cytometry. Surprisingly, IFN‐γ⁺ T cells, but not IFN‐γ^– T cells, induced osteoclastogenesis from monocytes, which was completely inhibited by adding osteoprotegerin and increased by adding anti‐IFN‐γ antibodies. The levels of both soluble and membrane type RANKL were elevated in IFN‐γ⁺ T cells. The ratio of CD4⁺ T cells expressing both IFN‐γ and RANKL in total CD4⁺ T cells from PBMC was elevated in RA patients. Contrary to our hypothesis, IFN‐γ⁺ human T cells induced osteoclastogenesis through the expression of RANKL, suggesting that Th1 cells play a direct role in bone resorption in Th1 dominant diseases such as RA.