Epigenetic Regulation of Host Immunity During Parasitic Infections: Mechanisms, Immune Evasion, and Therapeutic Opportunities.

INTRODUCTION Parasitic infections remain a major global health challenge involving complex interactions between pathogens and host immunity. Emerging evidence indicates that epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs, critically regulate immune responses and influence host susceptibility, resistance, and disease progression.

Methods

This review synthesizes current evidence on epigenetic regulation of host immunity during parasitic infections, focusing on mechanisms underlying immune activation, immune evasion, host susceptibility, and parasite persistence. Emerging epigenetic biomarkers and therapeutic strategies targeting epigenetic pathways are also considered.

Results

Parasites can manipulate host epigenetic machinery to evade immune surveillance, suppress protective responses, and establish persistent infections. Conversely, epigenetic regulation in immune cells modulates cytokine production, macrophage polarization, T-cell differentiation, and immune memory, thereby influencing infection outcomes. Parasite-derived epigenetic factors and non-coding RNAs may additionally contribute to immune modulation and immunopathology. Epigenetic signatures associated with disease severity and treatment response show potential as biomarkers, while targeting epigenetic pathways may enhance antiparasitic immunity.

Discussion

Epigenetic regulation represents a central mechanism governing host-parasite interactions. Integrating advanced approaches, including single-cell epigenomics and spatial transcriptomics, may clarify cell-specific mechanisms and identify novel biomarkers and therapeutic targets. These advances could support personalized strategies to improve antiparasitic treatment and disease outcomes.