TLR2 agonism suppresses myeloid leukemogenesis by reprogramming leukemia stem cells.

ABSTRACT:

Abstract

The consequences of activated innate immune signaling in acute myeloid leukemia (AML) is not well understood. Using ligands directed at the toll-like family receptors (TLR) in models of high-risk AML, we uncover that TLR2 ligands exert unique antileukemic effects that are distinct from other TLRs. Although TLR2 signaling broadly induces inflammatory gene expression in AML cells, at the single-cell level, cell-type-dependent, divergent transcriptional responses coordinate cellular outputs of proliferation, differentiation, cell death, and activation of immune cell function. TLR2 ligands were the only TLR agonists capable of extending survival of AML-bearing mice through leukemia stem cell (LSC) reprogramming that elevated major histocompatibility complex (MHC) class II surf

SUBMITTER: Lawler ME 

PROVIDER: S-EPMC12666352 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature