Human Leukocyte Antigen Determinants in Myocarditis and Dilated Cardiomyopathy

Figures

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  Fig. 1. Antigen presentation differences between HLA class I and class II molecules. This diagram contrasts the antigen processing and presentation pathways of HLA Class I and Class II molecules. HLA Class I presents endogenous viral peptides to cytotoxic CD8⁺ T cells, whereas HLA Class II presents exogenous peptides from extracellular bacteria to helper CD4⁺ T cells. The differential antigen presentation underscores the distinct roles of HLA classes in orchestrating immune responses relevant to myocarditis pathogenesis

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  Fig. 2. Mechanistic pathways by which HLA polymorphisms influence myocarditis and progression to dilated cardiomyopathy (DCM). HLA-dependent antigen presentation shapes antiviral clearance and autoimmune susceptibility by regulating CD4⁺ and CD8⁺ T-cell activation, cytokine amplification, and immune cell infiltration. High-affinity HLA variants promote persistent inflammation, autoreactive T-cell expansion, and autoantibody production, leading to myocardial injury, fibrosis, and progression to DCM

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  Fig. 3. HLA-restricted molecular mimicry in autoimmune myocarditis. Viral infection of cardiomyocytes generates peptides (e.g., VP1) that share structural homology with cardiac self-antigens such as MYH6. Viral and homologous self-peptides are presented via HLA class I and II molecules, activating CD8⁺ and CD4⁺ T cells. Cross-reactive T-cell recognition leads to cytokine production, cytotoxic injury, and sustained inflammation, promoting myocardial damage, fibrosis, and progression to dilated cardiomyopathy (DCM)