Ontology highlight
ABSTRACT: Background
Serum amyloid A (SAA), an acute-phase pro-inflammatory protein, is overexpressed in several cancers and is involved in shaping pro-tumor responses. We have previously reported that lung cancer stem cells secrete SAA, which contributes to tumor progression by inhibition of TH1 immunity. Here, we extended our studies to examine the mechanism of SAA mediated immunosuppression in both antigen-presenting cells (APCs) and the subsequent activation of T cells.Methods & results
Using ex vivo co-culture systems and in vivo mice models, we found that SAA impaired dendritic cell and macrophage activation and drove macrophages toward an M2 phenotype with reduced antigen presentation. Lung cancer cells overexpressing SAA also consistently showed impai
SUBMITTER: Huang M
PROVIDER: S-EPMC12757294 | biostudies-literature | 2025
REPOSITORIES: biostudies-literature