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Aim: To study the influence of total glucosides of paeony (TGP) on the expression of peripheral blood programmed cell death protein 1 (PD‐1) and its ligand (PD‐L1) in patients with primary Sjögren's syndrome (pSS). Method: Ten patients with new‐onset pSS were selected as the experimental group and were treated with 1.8 g of TGP (the main ingredient is Radix Paeoniae Alba) daily for 3 months; furthermore, 10 physically healthy individuals were selected as the control group. Peripheral blood mononuclear cells were isolated, and flow cytometry was used to detect PD‐1 expression on the surface of CD4+ T and CD8+ T lymphocytes and PD‐L1 expression on the surface of CD14+ monocytes and CD19+ B cells before and after treatment in the experimental and control groups. Furthermore, plasma levels of soluble PD‐1 (sPD‐1), interleukin (IL)‐10, and IL‐17A were also determined using enzyme‐linked immunosorbent assay. Results: The PD‐1 expression on the surface of CD4+ T and CD8+ T lymphocytes in the peripheral blood of patients with pSS were significantly higher than in the control group (P < 0.001). However, PD‐L1 expression on the surface of CD14+ monocytes declined but not significantly (P > 0.05), and PD‐L1 expression on the surface of CD19+ B cells increased significantly (P < 0.001). Moreover, sPD‐1 and IL‐17A levels in the plasma of the experimental group were significantly higher than in the control group (P < 0.001), but the IL‐10 level was significantly lower than in the control group (P < 0.001). After TGP treatment, PD‐1 expression on the surface of CD4+ T and CD8+ lymphocytes in the peripheral blood of patients with pSS had decreased significantly (P < 0.001); the PD‐L1 expression on the surface of CD19+ cells had decreased significantly (P < 0.001); and the PD‐L1 expression on the surface of CD14+ monocytes did not differ significantly (P > 0.05). Furthermore, the levels of sPD‐1 and IL‐17A in plasma had decreased (P < 0.01) and IL‐10 levels had increased after TGP treatment (P < 0.01). Conclusion: PD‐1/PD‐L1 molecules expressed on the surface of T cells, B cells, and monokaryon participated in the pathogenesis and development of SS through interactions. Therefore, TGP, which may increase the expression of PD‐1 and its relevant ligand PD‐L1 in the peripheral blood mononuclear cells, may play a role in the pathogenesis and development of SS through the PD‐1/PD‐L1 pathway by regulating regulatory T cells/T helper cell 17. [ABSTRACT FROM AUTHOR]