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Erucic acid improves the pregnancy complicated with systemic lupus erythematosus by inhibiting the effector function of CD8+ T cell

ABSTRACT: Pathogenic CD8+ T cells are closely related to the development of systemic lupus erythematosus. Erucic acid (EA) has been proved to have anti-inflammatory activity. However, whether EA can regulate pathogenic CD8+ T cells function in pregnancy complicated with systemic lupus erythematosus (pSLE) has not been investigated. In our study, we detected enhanced CD8+ T cell effector function and decreased EA levels in patients with pSLE compared to healthy pregnancy control. Plasma EA levels were negatively correlated with the severity complications of pSLE. In blood from patients with pSLE, EA inhibited the effector function of CD8+ T cells and the maintenance of stem cell-like memory CD8+ T cells. Mechanically, EA inhibited STAT3 phosphorylation and promoted ferroptosis, which contributed directly to the attenuated effector function of CD8+ T cells in pSLE. Moreover, EA supplementation in pregnant MRL/lpr mice inhibited the effector function of uterine CD8+ T cells and alleviated placental pathological damage. Our findings reveal the modulatory effects of EA on pathogenic CD8+ T cells from an immune response perspective, thus providing new insights into therapeutic strategy for patients with pSLE.

ORGANISM(S): Homo sapiens

PROVIDER: GSE222565 | GEO | 2025/01/01

REPOSITORIES: GEO

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Project description:Background/Purpose: Systemic lupus erythematosus (SLE) is a complex multi-system autoimmune disease of uncertain etiology. Patients from different ancestral backgrounds demonstrate differences in clinical manifestations and autoantibody profiles. In this study we examined genome-wide transcriptional patterns in major immune cell subsets across different ancestral backgrounds. Methods: Peripheral blood was collected from 21 African-American (AA) and 21 European-American (EA) SLE patients, 5 AA controls, and 5 EA controls. CD4+ T-cells, CD8+ T-cells, monocytes and B cells were purified by flow sorting. Each cell subset from each subject was run on an Illumina HumanHT-12 V4 expression BeadChip array (n=208 arrays). Differentially expressed genes (DEGs) were determined by comparing cases and controls of the same ancestral background. Results: The overlap in DEG lists between different cell types from the same ancestral background was very modest (<1%). Typically between 5-10% of DEGs were shared when comparing the same cell type between different ancestral backgrounds (for ex. CD20 AA vs. CD20 EA). Quantitative measurement of global IFN-stimulated gene (ISG) expression revealed that AA subjects demonstrated more concordance across all studied cell types. Two subgroups of patients were identified based on the ISG expression profiles. One subgroup showed higher ISGs expression in all cell types, and the other subgroup had higherISG expression only in T and B lymphocytes but not in monocytes. The correlation of ISG expression with medication data revealed that only the B cells had lower ISG expression in patients taking immunosuppressants, while ISG expression in the other cell types did not differ based upon medication use. Conclusion: We find striking differences in gene expression between different immune cell subsets and between ancestral backgrounds in SLE patients. The IFN signature is diverse, with different transcripts represented in different cell populations, and signature-positive cell subsets differed in EA vs. AA patients. We also find that treatment with the immunosuppressive agents correlates with the down-regulation of B cell ISG expression, and this was not observed in other cell types. Peripheral blood was collected from 21 African-American (AA) and 21 European-American (EA) SLE patients, 5 AA controls, and 5 EA controls. CD4+ T-cells, CD8+ T-cells, monocytes and B cells were purified by flow sorting. Each cell subset from each subject was run on an Illumina HumanHT-12 V4 expression BeadChip array (n=208 arrays).

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Erucic acid improves the pregnancy complicated with systemic lupus erythematosus by inhibiting the effector function of CD8+ T cell

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