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Updated: Jan 29, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

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Dendritic cells modulate c-kit expression on the edge between activation and death.

Sonia Simonetti^1,2, Amairelys B Barroeta Seijas^1,2, Ambra Natalini^1,2

¹Institute of Molecular Biology and Pathology, National Research Council (CNR), Rome, Italy.

European Journal of Immunology

|February 14, 2019

Summary

Stimuli mimicking bacterial and viral nucleic acids inhibit c-kit expression in dendritic cells (DCs), impairing stem cell factor (SCF) pro-survival signaling and impacting immune responses.

Keywords:

CpG PolyI:C Stem cell factor conventional dendritic cell subsets dendritic cell survival

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Evaluation of Caspase Activation to Assess Innate Immune Cell Death

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Published on: January 20, 2023

Area of Science:

Immunology
Cell Biology

Background:

Dendritic cells (DCs) are crucial for immune responses and tolerance.
The role and regulation of c-kit expression in DCs remain unclear.
Stem cell factor (SCF) signaling through c-kit supports DC survival.

Purpose of the Study:

To investigate the functional role of c-kit in DCs.
To determine how bacterial and viral nucleic acid mimics affect c-kit expression and function in DCs.
To elucidate the impact of c-kit down-regulation on DC survival and immune modulation.

Main Methods:

In vitro and in vivo studies using mouse bone marrow-derived DCs (BMdDCs) and spleen DCs.
Treatment with CpG and PolyI:C to mimic bacterial and viral nucleic acids.
Analysis of c-kit expression, mRNA levels, and phospho-AKT.
Experiments in IFNAR1-/- mice to assess the role of the IFN-I pathway.
Assessment of DC survival and cytokine production (IL-6, IL-12) with and without exogenous SCF.

Main Results:

CpG and PolyI:C significantly inhibited c-kit expression and mRNA in BMdDCs and spleen DCs.
The IFN-I pathway was essential for c-kit down-regulation in cDC1s, partially contributing in cDC2s.
SCF-mediated pro-survival signaling was impaired following CpG/PolyI:C treatment.
CpG/PolyI:C induced spleen DC death when SCF was provided, despite transient increases in IL-6 and IL-12.
Unstimulated DCs with high c-kit expression showed enhanced survival with SCF.

Conclusions:

Down-modulation of c-kit is a significant, previously unrecognized aspect of DC responses to CpG and PolyI:C.
Regulation of c-kit expression influences DC survival and modulates immune responses.
This finding offers new insights into the mechanisms controlling DC behavior during infection.