fig3

Figure 3. Metabolic microenvironment, immune evasion, and microbiome axis in AML. Bone marrow niche model showing AML blasts/LICs interacting with stromal cells via mitochondrial-transferring tunneling nanotubes, spatially heterogeneous metabolites (glucose/lactate perivascularly; 2-HG/kynurenine hypoxic zones), and immunosuppressive pathways (ARG2/IDO1 depleting arginine/tryptophan, impairing PD-1⁺TIM-3⁺ T cells and CAR-T). Gut microbiome-derived short-chain fatty acids (SCFAs; butyrate/propionate) modulate systemic HSCs, epigenetics, and therapy responses. Figure generated using AI-based tools and finalized by the authors in Microsoft PowerPoint. AML: Acute myeloid leukemia; LICs: leukemia-initiating cells; HSCs: hematopoietic stem cells; CAR-T: chimeric antigen receptor-T; AI: artificial intelligence.