AI Article Synopsis
- This study investigates how high levels of lipids and proteins related to cardiometabolic diseases affect the immune function of plasmacytoid dendritic cells (pDCs).
- The researchers found that exposure to oxidized low-density lipoproteins (oxLDL) causes lipid accumulation in pDCs, hindering their maturation and activation, which is crucial for effective immune responses.
- Ultimately, the research highlights how dyslipidemia negatively impacts pDC responses to pathogens, suggesting a potential link between metabolic disorders and compromised immune defense.
Article Abstract
Background: Pathogens or trauma-derived danger signals induced maturation and activation of plasmacytoid dendritic cells (pDCs) is a pivotal step in pDC-dependent host defense. Exposure of pDC to cardiometabolic disease-associated lipids and proteins may well influence critical signaling pathways, thereby compromising immune responses against endogenous, bacterial and viral pathogens. In this study, we have addressed if hyperlipidemia impacts human pDC activation, cytokine response and capacity to prime CD4 T cells.
Methods And Results: We show that exposure to pro-atherogenic oxidized low-density lipoproteins (oxLDL) led to pDC lipid accumulation, which in turn ablated a Toll-like receptor (TLR) 7 and 9 dependent up-regulation of pDC maturation markers CD40, CD83, CD86 and HLA-DR. Moreover, oxLDL dampened TLR9 activation induced the production of pro-inflammatory cytokines in a NUR77/IRF7 dependent manner and impaired the capacity of pDCs to prime and polarize CD4 T helper (Th) cells.
Conclusion: Our findings reveal profound effects of dyslipidemia on pDC responses to pathogen-derived signals.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9139034 | PMC |
| http://dx.doi.org/10.3390/biomedicines10051152 | DOI Listing |
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