Evaluating IL-17A and TNF-α as immunological predictors of recurrent abortion in systemic lupus erythematosus patients with toxoplasmosis: A case-control study

Background. Toxoplasma gondii is a globally distributed intracellular parasite that causes human toxoplasmosis in approximately one third of the population. Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by heterogeneity in clinical manifestations and an imbalance in immune tolerance. When present together in SLE, these conditions may cause marked dysregulation of immune responses, leading to greater disease severity than when each occurs alone. Objective. This pilot case control study aimed to assess the roles of IL 17A and TNF α and to determine which cytokine is more influential in the severity of SLE among women infected with toxoplasmosis (cases) compared with healthy women (controls), including the association with recurrent abortions. Subjects and methods. Eighty nine women were enrolled in two categories: 44 with SLE and seropositive toxoplasmosis (cases) and 45 healthy controls. Serum IL 17A and TNF α were measured using commercial human ELISA kits. Statistical analyses included independent samples t tests, Cohen’s d for effect size, and Spearman’s rank correlation, with p < 0.01 considered significant. Results. IL 17A and TNF α levels were significantly higher in cases than in controls (729.9 vs 465.3 pg/mL and 98.5 vs 30.6 pg/mL, respectively; p = 0.001). IL 17A levels (mean ± SE) were significantly higher in SLE women with recurrent abortion (814.83 ± 11.5 pg/mL) than in those without (578.53 ± 12.7 pg/mL; p < 0.001), suggesting a relationship with increased recurrent abortion frequency. TNF α levels did not differ significantly between women with vs without recurrent abortion. Conclusion. Accidental toxoplasmosis may be a risk factor for increased disease severity in SLE through elevated serum IL 17A and TNF α. Among immunological indicators, IL 17A showed the strongest association with recurrent abortions in SLE with toxoplasmosis, followed by anti Toxoplasma IgG, ANA, and anti dsDNA, whereas TNF α and anti Toxoplasma IgM showed no effect. Main limitation: the study lacked SLE only and toxoplasmosis only comparator groups.