ArticleAmerican journal of physiology. Cell physiology2024
Implications of IFNγ SNP rs2069705 in primary Sjögren's syndrome: transcriptional activation and B cell infiltration.
Article in American journal of physiology. Cell physiology, 2024. 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, 2 citations in OpenAlex.
- IFN-γ-Associated Signaling Networks in Interstitial Lung Disease Associated With Sjögren's Disease.Immunity, inflammation and disease · 2026Review
- A Bone-Protective Role for IFN-γ? Evidence from Genetic Association and Osteoblast Functional Assays in Postmenopausal Osteoporosis.International journal of molecular sciences · 2026Article
- The pathogenic role of double-negative B cells in autoimmune diseases.Frontiers in immunology · 2026Review
- A comprehensive review of Sjögren's syndrome: Classification criteria, risk factors, and signaling pathways.Heliyon · 2024Review
- Transcriptomics explores potential mechanisms for the development of Primary Sjogren's syndrome to diffuse large B-cell lymphoma in B cells.BMC immunology · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary Sjögren's syndrome (pSS) is characterized by its autoimmune nature. This study investigates the role of the IFNγ SNP rs2069705 in modulating the susceptibility to pSS. Differential expression of IFNγ and BAFF was analyzed using the GEO database's mRNA microarray GSE84844. Genotyping of the IFNγ SNP rs2069705 was conducted via the dbSNP website. The JASPAR tool was used for predicting transcription factor bindings. Techniques such as dual-luciferase reporter assays, Chromatin immunoprecipitation, and analysis of a pSS mouse model were applied to study gene and protein interactions. A notable increase in the mutation frequency of IFNγ SNP rs2069705 was observed in MNCs from the exocrine glands of pSS mouse models. Bioinformatics analysis revealed elevated levels of IFNγ and BAFF in pSS samples. The model exhibited an increase in both CD20+ B cells and cells expressing IFNγ and BAFF. Knocking down IFNγ resulted in lowered BAFF expression and less lymphocyte infiltration, with BAFF overexpression reversing this suppression. Activation of the Janus kinase (JAK)/STAT1 pathway was found to enhance transcription in the BAFF promoter region, highlighting IFNγ's involvement in pSS. In addition, rs2069705 was shown to boost IFNγ transcription by promoting interaction between its promoter and STAT4. SNP rs2069705 in the IFNγ gene emerges as a pivotal element in pSS susceptibility, primarily by augmenting IFNγ transcription, activating the JAK/STAT1 pathway, and leading to B-lymphocyte infiltration in the exocrine glands.
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