Abstract
Background. Toxoplasma gondii is an intracellular parasite with a global prevalence, capable of establishing chronic infections in humans. While T. gondii is traditionally considered asymptomatic in immunocompetent individuals, emerging evidence suggests that it may contribute to immune dysregulation, potentially triggering or exacerbating autoimmune processes. Therefore, this study investigated the relationship between T. gondii infection and the presence of anti-nuclear antibodies (ANA).
Methods. A total of 284 blood samples, including 142 ANA-positive individuals and 142 healthy controls, were analyzed for the immunoglobulin (Ig) G and IgM antibodies of T. gondii using an enzyme-linked immunosorbent assay. Additionally, polymerase chain reaction (PCR) was performed on IgM-positive samples to confirm the presence of T. gondii DNA.
Results. The results demonstrated the significantly higher prevalence of T. gondii IgG antibodies in ANA-positive individuals (47.3%) compared to controls (11.3%) (P < 0.001), suggesting a potential link between chronic toxoplasmosis and immune dysregulation. While IgM positivity was rare, PCR confirmed the presence of T. gondii DNA in an IgM-positive ANA patient.
Conclusion. Overall, these findings support the hypothesis that persistent T. gondii infection may influence autoimmune pathways, warranting further investigation into its role as an environmental factor in autoimmunity.
Practical Implications. The findings suggest that chronic T. gondii infection may be linked to the increased production of ANA and immune dysregulation. This association could position T. gondii as an environmental factor in the onset or exacerbation of autoimmune diseases. In addition, the results highlight the importance of screening and monitoring T. gondii infection in individuals with autoimmune markers, such as ANA, and underscore the need for further research into the underlying mechanisms. It is hoped that such insights pave the way for targeted preventive and therapeutic strategies in autoimmune disorders.