Decoding IGLL5 Mutation‐Mediated BCR Signaling: A Novel Mechanism of CD8 ⁺ T Cell Exhaustion and Ocular MALT Lymphoma Progression

T cell recruitment, and an exhaustion-associated dysfunctional phenotype that may contribute to an immune-tolerant microenvironment. Pharmacologic inhibition further shows that combined BTK inhibitor and rituximab treatment suppresses IGLL5-associated BCR activation. Together, these findings support a mutation-associated mechanism in a subset of OAML and nominate IGLL5-related signaling as a potential therapeutic vulnerability.