Introduction: Rheumatoid arthritis (RA) combined with hashimoto thyroiditis (HT) is an important cause of various fatal comorbidities of RA. There is no precise conclusion about the cause of this disease. Methods: Peripheral blood and synovial tissue were collected from healthy participants, patients with RA, and patients with both RA and HT. Immunofluorescence staining and Pearson correlation analysis were used to detect the levels of gamma delta TCR and the correlation between IL-17 and p-STAT3, respectively. ELISA, chemiluminescence assays, qRT-PCR and Western blot were performed to detect the levels of IgG, IgM, IFN-gamma, IL-1 beta, TNF-alpha, Tg-Ab, Tpo-Ab, IL-17, IL-2, p-SATA3, and STAT3, respectively. Results: There was increased proportion of gamma delta T cells, IL-17, and p-STAT3 levels in RA and HT patients. IL-17 was positively correlated with p-STAT3. gamma delta T cells significantly promoted the expression of IgG, Tg-Ab, Tpo-Ab, and IL-17. When gamma delta T and human fibroblast-like synoviocytes (FLSs) were co-cultured, the levels of IL-2, IFN-gamma, IL-1 beta, TNF-alpha, and IL-17 were increased, and the IL-17/STAT3 signaling pathway was activated. When IL-17-silenced gamma delta T cells and STAT3-silenced FLSs were co-cultured, the levels of IL-1 beta and TNF-alpha in FLSs were significantly decreased. Furthermore, when STAT3-silenced FLSs were added to the co-culture medium of B cells and gamma delta T cells, the levels of IL-1 beta and TNF-alpha were also decreased significantly. Conclusion: gamma delta T cells induced RA directly or by stimulating B cells to activate STAT3 through IL-17.