{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T15:18:25Z","timestamp":1791818305788,"version":"4.3.4"},"reference-count":240,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,7,23]],"date-time":"2025-07-23T00:00:00Z","timestamp":1753228800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Immunotherapy has emerged as a cornerstone strategy for augmenting therapeutic efficacy in acute myeloid leukemia (AML). The immunosuppressive AML microenvironment, characterized by profound immune dysfunction, critically impairs anti-leukemic immune surveillance. This immunologically hostile niche is principally governed by specialized immunosuppressive cell populations\u2014notably regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), leukemia-associated macrophages (LAMs), and regulatory B cells (Bregs)\u2014which collectively establish an immune-privileged sanctuary for leukemic cells. This review critically examines three fundamental aspects of these immunosuppressive regulators in AML pathogenesis: (1) their recruitment dynamics within the leukemic niche, (2) the molecular mechanisms underlying their immunosuppressive functions, and (3) current and emerging therapeutic approaches designed to neutralize their inhibitory effects. 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