Follistatin-Like Protein-1 Upregulates Dendritic Cell-Based Immunity in Patients with Nasopharyngeal Carcinoma

Wang Hong et al., Journal of Interferon & Cytokine Research (2017) - PMID: 29135371

Product(s) used in this publication: PepMix™ Peptide Pools


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.

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