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Objectives Tenascin-C (TNC) is a large extracellular matrix glycoprotein that plays an important role in the regulation of cell adhesion, migration, and immune response. Its expression is minimal in healthy tissues, but increases significantly during inflammation and tissue repair. In systemic lupus erythematosus (SLE), TNC acts as an endogenous activator of innate immunity, binding to TLR4 and stimulating the production of cytokines such as IL-6 and TNF-α, thereby contributing to chronic inflammation and tissue damage. The rs2104772 polymorphism within the TNC gene may affect protein expression and function, potentially altering the inflammatory response in SLE patients. This study aimed to explore the potential impact of the TNC rs2104772 polymorphism on clinical manifestations of SLE.Methods Our study included 96 adult SLE patients diagnosed and treated at the Clinic of Allergy and Immunology, University Clinical Center of Serbia. Genotyping for the TNC rs2104772 polymorphism was performed using TaqMan assays.Results Genotyping of the TNC rs2104772 polymorphism showed that 34 (35.4%) patients harboured the TT genotype, 46 (47.9%) had the TA genotype, and 16 (16.7%) patients had the AA genotype. The analysis showed a significantly higher frequency of fatigue (70.6% vs 43.5%; p=0.018), oral ulceration (42.4% vs 19.4%; p=0.028), nonerosive arthritis (100% vs 83.9%; p=0.013) and tenosynovitis (47.1% vs 21%; p= 0.011) in patients with TT genotype for TNC rs2104772 polymorphism compared to carriers of the A allele. At the same time, renal involvement was more frequent in A allele carriers (32.3% vs 12.1%; p=0.046).Conclusions The results of this study indicate an association between the TNC rs2104772 polymorphism and the clinical expression of SLE, suggesting a possible role of this genetic variant in disease pathogenesis.