The role of STAT3 signaling in the activity of dendritic cells (DC) has been recently revealed in a publication by Okada et al.
Dendritic cells (DCs) are important innate and adaptive immune effectors, and have a key role in antigen presentation and T-cell activation. Different lineages of DCs can be developed from hematopoietic progenitors following cytokine signaling (e.g. IL-15, IL-4), and the various lineages of DCs display distinct morphology, phenotype and functions.
IL-15-derived DCs elicited greater antigen-specific, primary and secondary CD8 and CD4 T-cell responses than IL-4-derived DCs. Also, IL-15 DCs secrete substantial amounts of proinflammatory cytokines, including IL-6, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNFα), which helps polarise a strong T-cell response.
The publication uses specific inhibitors to STAT3 and p38 MAPK pathways and reveals that the STAT3 signaling, but not p38 MAPK signaling, contributes to IFN-γ production in DCs. Therefore, while IL-15 does not promote the STAT signaling in DCs, the increased STAT3 activity after LPS/TNFα treatment of the IL-15 DCs has a 
key role in their high IFN-γ effector activities.
Cytokine profile of the IL-15 DCs was achieved using the Q-plex technology, performed at Quansys laboratories in the USA. Researchers in Europe can also benefit from this technology (and other biomarker profiling technologies, e.g. to unravel signaling pathways) at tebu-bio laboratories located near Paris.
No need to send your samples on a journey overseas!
