Follistatin‐like protein 1 (FSTL1) is a newly characterized protein that can regulate the immune response in various ways. Dendritic cells (DCs) are central to immune regulation. In this study, we explored the impact of FSTL1 on DC activity in nasopharyngeal carcinoma (NPC) patients. The surface expression of CD40, CD86, and HLA‐DR on DCs was analyzed and showed significantly elevated expression levels, indicating DC maturity. After FSTL1 was added to DCs collected from NPC patients (n = 50), controls (n = 47), and healthy donors (n = 10), interferon γ secretion and T‐cell receptor expression in cytotoxic T lymphocytes were also investigated. In the experimental groups, the expression of the critical immune protein nuclear factor (NF)‐κb was upregulated, whereas Jun N‐terminal kinase (JNK) was downregulated. Our findings demonstrate that FSTL1 plays a critical role in immune regulation, enhancing the antigen presentation ability of DCs by up‐regulating NF‐κb expression and down‐regulating JNK expression.

Follistatin-like protein-1 (FSTL1) is an inflammatory factor that can induce an inflammatory response and is expressed in cancers. However, little is known about its content and function in nasopharyngeal carcinoma (NPC). Interleukin (IL)-12 and IL-4 are primarily secreted by dendritic cells (DCs) and activated T lymphocytes, respectively; these factors can induce Th cell differentiation and cytotoxic lymphocyte production, both of which facilitate tumors through the STAT4 and STAT6 pathways, respectively. In this study, the relationship between FSTL1 and both IL-12 and IL-4 as well as the functional mechanism of these cytokines was explored. Enzyme-linked immunosorbent assay, flow cytometry, and Western blotting were used to assess the levels of key inflammatory factors and DC markers as well as elucidate the mechanism by which FSTL-1 mediates and exerts it antitumor effects. The results revealed that serum FSTL1 and IL-12 levels were significantly decreased in NPC patients compared with those in the control group (P < 0.05); conversely, IL-4 levels were increased (P < 0.05). Supernatants from the experimental groups (EGs) contained higher IL-4 and IL-12 levels than those from the control groups (P < 0.05). Additionally, phosphorylated-STAT6 and phosphorylated-STAT4 were increased in the EGs (P < 0.05). These results suggest that DC-mediated immunity was activated by FSTL1, which leads to an increase of IL-12 and IL-4 production and consequently activates the STAT4 and STAT6 pathways through upregulation of STAT4 and STAT6 phosphorylation, respectively.