Objective To investigate the proportional change of CD56+ T cells in peripheral blood of patients with rheumatoid arthritis (RA) and the expression of T cell immunoglobulin and immune receptor tyrosine inhibitory motif domain (TIGIT) on the surface of CD56+ T cells, and to explore the effect of TIGIT on CD56+ T cell function in RA. Methods Fifty patients with RA and twenty healthy controls were selected. Flow cytometry was used to determine the proportion of CD56+ T cells in peripheral blood, and the correlation between the resulting cell ratio and clinical indicators of the disease was analyzed. Flow cytometry was used to measure the expression level of TIGIT in peripheral blood CD56+ T cells in RA patients. Density gradient centrifugation was used to isolate peripheral blood mononuclear cells which were subsequently cultured in vitro. The proportion of CD56+ T cells expressing Interferon-γ (IFN-γ) and Interleukin-17A (IL-17A) in peripheral blood of RA patients were measured. The differential expression of IFN-γ and IL-17A in TIGIT- CD56+ T cells and TIGIT+ CD56+ T cells was investigated. The serum IL-17A levels in RA patients were assayed by ELISA. Results Compared with the healthy controls, the proportion of CD56+ T cells in peripheral blood was reduced in RA patients, and the proportion of CD56+ T cells expressing IL-17A was significantly reduced; Serum IL-17A concentration was elevated in RA patients. CD56+ T cells in RA patients were with higher expression of TIGIT molecules, and IFN-γ was mainly derived from TIGIT- CD56+ T cells. There was no significant difference between the proportion of TIGIT- CD56+ T cells and TIGIT+ CD56+ T cells expressing IL-17A. Conclusion Abnormal expression of TIGIT affects cytokine secretion function of CD56+ T cells, which in turn participates in the RA disease progression. And IFN-γ is mainly derived from TIGIT- CD56+ T cells. However, TIGIT may not affect the IL-17A secretion level of CD56+ T cells.