ArticleFrontiers in immunology2019
Silencing SOCS1 via Liposome-Packed siRNA Sustains TLR4-Ligand Adjuvant.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Unravelling the druggability and immunological roles of the SOCS-family proteins.Frontiers in immunology · 2024Review
- Magnetically responsive nanoplatform targeting circRNA circ_0058051 inhibits hepatocellular carcinoma progression.Drug delivery and translational research · 2023Article
- Nanoparticle-MediatedACS nano · 2021Article
- Suppressor of cytokine signaling 1 inhibits the maturation of dendritic cells involving the nuclear factor kappa B signaling pathway in the glioma microenvironment.Clinical and experimental immunology · 2020Article
- The effect ofAging · 2020Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infectious diseases remain one of the leading causes of death worldwide. Vaccination is a powerful instrument to avert a variety of those by inducing a pathogen-specific immune response and ensure a long-lasting protection against the respective infection. Nevertheless, due to increasing numbers of immunocompromised patients and emergence of more aggressive pathogens existing vaccination techniques are limited. In our study we investigated a new strategy to strengthen vaccine adjuvant in order to increase immunity against infectious diseases. The strategy is based on an amplification of Toll-like receptor 4 (TLR4) -induced activation of antigen-presenting cells (APCs) by turning off a powerful endogenous inhibitor of APC-activation. TLR4 signaling induces the release of cytokines that bind autocrine and paracrine to receptors, activating the Janus kinase (JAK) 2/signal transducers and activators of transcription (STAT) 3 cascade. Subsequently, STAT3 induces expression of suppressor of cytokine signaling (SOCS) 1 that terminates the inflammatory response. In the approach, TLR4-adjuvant monophosphoryl lipid A (MPLA)-stimulated monocyte-activation is reinforced and sustained by silencing SOCS1 via lipid nanoparticle-enclosed siRNA (L-siRNA). L-siRNA is transported into primary cells without any toxic side effects and protected from early degradation. Through lipid core-embedded functional groups the lipid particle escapes from endosomes and releases the siRNA when translocated into the cytoplasm. SOCS1 is potently silenced, and SOCS1-mediated termination of NFκB signaling is abrogated. Consequently, the MPLA-stimulated activation of APCs, monitored by release of pro-inflammatory cytokines such as IL-6, TNFα, and IL-1β, upregulation of MHC class II molecules and costimulatory CD80/CD86 is strongly enhanced and prolonged. SOCS1-silenced APCs, pulsed with liposomal tetanus light chain toxin (TeTxLC) antigen, activate autologous T cells much more intensively than SOCS1-expressing cells. Importantly, expansion of cocultured CD4
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