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Genome-wide analysis of atypical NK cell subset in mouse model of Systemic Lupus Erythematosus (SLE)

ABSTRACT: Exploratory study to identify genome-wide changes in expression between conventional NK cells isolated from B6 WT and NK1.1+ cells from TLR7tg mice

ORGANISM(S): Mus musculus

PROVIDER: GSE63829 | GEO | 2014/12/04

SECONDARY ACCESSION(S): PRJNA269177

REPOSITORIES: GEO

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Genome-wide analysis of atypical NK cell subset in mouse model of Systemic Lupus Erythematosus (SLE)

Project description:Exploratory study to identify genome-wide changes in expression between conventional NK cells isolated from B6 WT and NK1.1+ cells from TLR7tg mice Isolated splenic NK1.1+ cells are compared between B6 WT and TLR7tg mice

2014-12-04 | E-GEOD-63829 | biostudies-arrayexpress

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Project description:Objectives: Natural Killer (NK) cell dysfunction contributes to systemic lupus erythematosus (SLE) pathogenesis, but its underlying mechanisms remain poorly understood. This study investigates immunometabolic alterations in NK cells from SLE patients and explores therapeutic strategies for their restoration. Methods: We characterized mitochondrial structure and function in NK cells from the peripheral blood of SLE patients and healthy controls using flow cytometry, electron microscopy, and proteomics. Key mitophagy-related gene expressions were quantified using qPCR. The therapeutic effects of hydroxychloroquine (HCQ) on mitochondrial recycling and NK cell function were assessed in vitro. Results: SLE NK cells were characterized by an accumulation of enlarged, hyperpolarized mitochondria with cristae disorganization, and reduced mitophagy. Impaired lysosomal acidification and mtDNA extrusion into the cytosol were also observed. Treatment with hydroxychloroquine restored lysosomal pH, mitochondrial recycling, and NK cell effector functions, including cytokine production and cytotoxicity. Conclusions: This study identifies mitochondrial recycling dysfunction as a driver of NK cell abnormalities in SLE and highlights the potential of HCQ to restore NK cell functionality. These findings provide new insights into the immunometabolic mechanisms underlying SLE and suggest avenues for targeted therapeutic interventions.

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