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This research investigates the expression profile of lncRNA NRIR in patients with antiphospholipid syndrome (APS) and its relationship to immune signaling pathways.

April 1, 2026Open Access

Proof-of-concept evidence for lncRNA NRIR downregulation in antiphospholipid syndrome and its obstetric subtype

Key Points

This research investigates the expression profile of lncRNA NRIR in patients with antiphospholipid syndrome (APS) and its relationship to immune signaling pathways.
Conducted a cross-sectional exploratory study using CD14-enriched peripheral blood monocytes.
Quantified NRIR expression with reverse transcription-quantitative PCR.
Compared NRIR expression between APS patients and healthy controls, focusing on obstetric and non-obstetric subtypes.
Performed in silico analysis for protein-protein interactions and pathway enrichment.
NRIR expression significantly reduced in APS patients compared to healthy controls.
Obstetric APS (OAPS) patients showed less downregulation of NRIR than non-obstetric APS (NOAPS) patients.
Network analysis indicated NRIR's connection to a STAT1-centered IFN-enriched module, suggesting its involvement in immune responses.

Abstract

Background/Objetive: Long non-coding RNAs (lncRNAs) regulate immune signaling pathways, including interferon (IFN)-mediated responses implicated in antiphospholipid syndrome (APS). The IFN-inducible lncRNA NRIR (AC017076.5) exhibits context-dependent regulatory functions and has been associated with modulation of STAT1/STAT2 activation in human monocytes. Its expression profile in APS remains unexplored. Method: In this cross-sectional exploratory study, NRIR expression was quantified by reverse transcription-quantitative PCR in CD14-enriched peripheral blood monocytes from APS patients and age-and sex-matched healthy controls. Relative expression was calculated using the 2 -Ct method with GAPDH as endogenous control. Subgroup analyses compared obstetric APS (OAPS) and non-obstetric APS (NOAPS). Complementary in silico protein-protein interaction and pathway enrichment analyses contextualized NRIR within IFN-related networks. Results: NRIR expression was significantly reduced in APS compared with controls. OAPS patients exhibited less pronounced downregulation than NOAPS, showing an intermediate expression pattern. Network analysis identified a STAT1-centered IFN-enriched module related to antiviral and type I IFN signaling, with NRIR positioned peripherally. Functional inferences remain hypothesis-generating due to sample size and absence of direct IFN measurements. Conclusion:NRIR is downregulated in peripheral monocytes from APS patients, with phenotype-dependent differences.Further mechanistic and IFN-integrated studies are required.

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