ArticleClinical and translational medicine2026
Lactate-induced metabolic reprogramming of TAMs impairs antigen presentation capacity via C/EBPα-CD74 axis in oral squamous cell carcinoma.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Review
- Drug-resistant bacterial infections in end-stage liver disease: immune imbalance and intervention advances.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundThroughout oral squamous cell carcinoma (OSCC) progression, tumor-associated macrophages (TAMs) lose their antigen-presenting capacity and anti-tumor function. The mechanisms that cause this dysfunction are not fully understood. CD74 is essential for antigen-presenting process, while little direct evidence describes its role in TAMs' immune function.
methodsWe integrated single-cell transcriptomic analysis, clinical cohort validation and CD74 conditional knockout mouse model to investigate the role of CD74 in TAMs during OSCC progression. Metabolomic analysis and mechanistic studies were performed to dissect how lactate-mediated metabolic reprogramming regulates CD74 expression.
resultsWe demonstrate that lactate accumulation in TME induces metabolic reprogramming of TAMs, which drives the acetylation of C/EBPα, and consequently suppresses CD74 expression. This downregulation of CD74 impairs the antigen-presenting capacity of TAMs, suppresses T cell activation, and ultimately promotes OSCC progression and recurrence.
conclusionsOur findings reveal the critical role of the lactate-C/EBPα-CD74 axis in shaping TAMs function, and provide potential therapeutic target for OSCC immunotherapy. KEY POINTS: CD74
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