Tnf, also known as Tumour necrosis factor α, is a classical pro-inflammatory cytokine [2]. It is ubiquitously present in the human body and plays a significant role in multiple physiological and pathological processes, including immunity, inflammation, and apoptosis [3,4]. TNF-α signals through binding to Types 1 and 2 TNF receptors (TNF-R1 and -R2), which are involved in various pathways [1].

Mice with genetic deletion of Tnf (Tnf+/- and Tnf -/-) were used to study myocarditis. In these models, Tnf+/- and Tnf -/- mice immunized with α -myosin heavy chain peptide showed reduced myocarditis incidence, but susceptible animals developed extensive heart inflammation. In the transgenic T cell receptor (TCRM) model, defective Tnf production was associated with increased mortality at a young age due to cardiomyopathy and cardiac fibrosis. These findings suggest that Tnf promotes myocarditis development by activating cardiac endothelial cells, but in established disease, it protects from exacerbating cardiac inflammation by inducing activation -induced cell death of heart -reactive effector CD4+ T cells [2].

In conclusion, Tnf is a crucial cytokine in inflammation and immunity. The study of Tnf knockout mouse models has revealed its complex role in myocarditis, highlighting both its pro -inflammatory and protective functions in the context of this disease. This contributes to understanding the basis of heart -related diseases and may provide insights for more targeted therapeutic approaches [2].