RNA alternative splicing (AS) has emerged as a central post-transcriptional mechanism driving antigenic diversity and immune escape.
First-pass extracted concept
RNA alternative splicing
Evidence Snippets
Supporting Sources
Linked Claims
Aberrant activity of splicing regulators disrupts canonical exon selection, leading to altered receptor signaling or secretion of soluble decoy isoforms that evade immune recognition.
Alternative-splicing-generated isoforms remodel surface antigen structure and function across therapeutic targets including CD19, CD20, CD22, EGFR/HER2, VEGF, and PD-1/PD-L1, thereby promoting resistance to monoclonal antibodies, antibody-drug conjugates, and immune checkpoint inhibitors.
RNA alternative splicing is presented as a central post-transcriptional mechanism driving antigenic diversity and immune escape in antibody-based cancer therapy contexts.
Understanding splicing-driven antigenic plasticity provides a framework for RNA-informed precision antibody therapies designed to restore antigen expression, overcome immune escape, and enhance durable clinical responses.