Presence of LILRB4 SNP rs1048801 modulates Acute Myeloid Leukemia progression and inhibits CD4+ T cells proliferation

• DOI: 10.1093/jleuko/qiaf052
• Publication Date: 2025-04-25T07:03:38Z
• Authors: Zhiyong Zhou; Yi Li; Di Wu; Yiliang Xiao; Shuyan Zeng; Qiuyun Xiao; Siqi Chen; Junpeng Ma; Xin Yuan; Jin Chen; Huiyun Peng

Abstract Leukocyte immunoglobulin-like receptor subfamily B member 4 (LILRB4), an emerging immune checkpoint molecule, exhibits therapeutic potential in acute myeloid leukemia (AML). While single nucleotide polymorphisms (SNPs) of genes have been extensively investigated AML, the association between LILRB4 genetic and clinical outcomes remains unexplored. We SNPs within immunoglobulin domain immunoreceptor tyrosine-based inhibitory motif (ITIM) regions 151 AML patients 203 controls. The rs1048801 G allele was significantly associated with increased mRNA expression, higher disease susceptibility, reduced overall survival. Functional studies revealed that enhanced cell proliferation colony formation. Furthermore, protein-protein interaction network analysis identified CD4 as a pivotal downstream mediator LILRB4. Flow cytometry elevated expression CD45+ leukocytes CD45+CD33+CD14+ monocytic cells from carriers, concomitant CD3+CD4+ T populations impaired proliferation. Collectively, these findings establish critical modulator progression through LILRB4-mediated CD4+ suppression, providing new insights for personalized strategies.