ArticleCancer management and research2026
TNFAIP3 Reprograms T Cell Exhaustion and Restores Anti-Leukemia Immunity in Acute Myeloid Leukemia.
Article in Cancer management and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Acute myeloid leukemia (AML) is an aggressive hematological malignancy that is associated with profound immune dysfunction. T-cell exhaustion is a major mechanism of immune evasion in AML; however, the key molecular regulators driving this process remain unclear. This study aimed to identify immunoregulatory genes associated with T cell exhaustion in AML and define their functional roles. Patients and Methods: Single-cell RNA sequencing (scRNA-seq) data from patients with AML and healthy donors were integrated to identify genes associated with T-cell exhaustion. TNFAIP3 was identified as a candidate hub gene and subsequently validated in peripheral T cells from 24 AML patients and 12 healthy donors using qRT-PCR and Western blotting. Functional studies were performed using lentivirus-mediated TNFAIP3 overexpression in patient-derived CD4+ and CD8+ T-cells. Apoptosis, immune checkpoint expression, cytokine production, and NF-κB signaling activity were assessed using pathway enrichment analyses. Results: scRNA-seq analysis revealed widespread immune remodeling in AML, with TNFAIP3 consistently downregulated in AML T cells. Reduced TNFAIP3 expression was confirmed at both the mRNA and protein levels in patients with AML. TNFAIP3 overexpression in CD4+ and CD8+ T cells attenuates apoptosis, reduces the expression of the immune checkpoint molecules PD-L1 and TIM-3, and promotes a pro-inflammatory cytokine profile characterized by increased IFN-γ and TNF-α production. Mechanistically, these effects were associated with the suppression of NF-κB signaling and enrichment of pathways related to immune synapse formation and T-cell receptor signaling. Conclusion: Our findings demonstrate that TNFAIP3 is a critical regulator of T cell dysfunction and exhaustion in AML. Downregulation of TNFAIP3 contributes to impaired anti-leukemic immunity, whereas its restoration enhances T-cell survival and effector function. TNFAIP3 therefore represents a promising therapeutic target for immune-based interventions aimed at restoring T-cell-mediated immunity in AML.
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