The present study revealed that individuals with MI exhibited significantly higher concentrations of anti-T. gondii antibodies compared to non-MI. The data further suggest that IFN-γ and TGF-β serve as critical biomarkers connected in the pathogenesis of MI. Our findings propose that T. gondii may contribute to the development of MI via immune-mediated inflammatory pathways. This observation indicates potential molecular similarities between the pathological elements of MI and the T. gondii pathogen. Moreover, the elevated expression of IFN-γ and TGF-β may offer a respected context for investigating the involvement of T. gondii in MI pathophysiology.
Jasim et al. (2026) studied this question.