Purpose <p>Breast cancer (BC) is the most prevalent female cancer globally. A key feature of cancer cells is a remarkable alteration in lipid composition, notably an enrichment in monounsaturated fatty acids. This change results from the upregulated expression of enzymes involved in fatty acid metabolism, such as stearoyl-CoA desaturase 1 (SCD1), which may affect immune-related responses.</p> Patients and methods <p>In the present study, 20 patients with luminal A BC and 20 healthy controls were included based on diagnostic criteria. Then, 10&#xa0;ml of peripheral blood was retrieved from each participant, and peripheral blood mononuclear cells (PBMCs) were isolated, pooled, and cultured in RPMI 1640 medium. The treatment and control groups were then treated with 3 µM of the SCD1 chemical inhibitor and DMSO, respectively, for 48&#xa0;h. The alteration in inflammatory markers IL-17 and TNF-α, anti-inflammatory markers IL-10 and TGF-β, inflammatory differentiation markers RORγt, and anti-inflammatory differentiation markers FOXP3 were assessed through Real-time PCR. Furthermore, the amount of the respective protein was measured through the enzyme-linked immunosorbent assay method.</p> Results <p>Chemical inhibition of SCD1 resulted in a significant downregulation of IL-17/TNF-α and upregulation of IL-10/TGF-β expression in the patient group. Additionally, a significant upregulation of FOXP3 was observed in BC patients after SCD1 inhibition. RORγt expression was also decreased in healthy individuals after SCD1 inhibition, with no effect on the patient group.</p> Conclusion <p>The results of this study suggest that SCD1 may act as a potential biomarker in the context of immune response.</p>