Background: The study of immune system dysregulation in systemic lupus erythematosus (SLE) has gained significant attention due to its complex pathophysiology, characterized by the involvement of various immune cell types, including B cells. Interferons, particularly type I IFN, play a crucial role in the inflammatory processes associated with SLE, influencing the activation and differentiation of B cells. Understanding the relationship between interferon status and B cell subpopulations is essential for elucidating the clinical manifestations of SLE and developing targeted therapies. This study aims to explore the characteristics of B cell subpopulations and their correlation with interferon activity in SLE patients, providing insights that may contribute to personalized treatment strategies.

Objectives: The aim of this study is to evaluate B cell subpopulations and the characteristics of interferon (IFN) status in patients with systemic lupus erythematosus (SLE) to clarify the relationship between immunological parameters and the clinical manifestations of the disease.

Methods: The analysis included 100 patients (82 women and 18 men) diagnosed definitively with SLE, with a mean age of 34 years, ranging from 16 to 60 years. The average disease duration was 7 years, with a SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) score of 8 points and a SLICC/ACR Damage Index (SDI) score of 2 points. Immunophenotyping of peripheral blood lymphocytes, including the determination of B cells, total memory B cell population, unswitched and switched memory B cells, transitional and naive B cells, and plasmablasts, was performed using multicolor flow cytometry. The IFN status was assessed through the expression of IFN-stimulated genes (MX1, RSAD2, EPSTI1) using real-time polymerase chain reaction (PCR).

Results: Two immunological “patterns” were identified: the predominant immune mechanism in the pathogenesis of SLE with predominant activation of type I IFN and with predominant activation of the B cell component of the immune system. The immune phenotype with type I IFN activation was associated with high immunological activity, predominant skin damage, and leukopenia, while the phenotype with predominant B cell activation was linked to damage in the kidneys and nervous system.

Conclusion: The results of this study suggest a wide variety of underlying immunological mechanisms in the pathogenesis of SLE. It is possible to identify several principal molecular “patterns” of disease pathogenesis, which should be considered when selecting effective “targeted” therapy. We encourage Latin American groups to conduct such characterizations of our patients.

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Acknowledgements: NIL.

Disclosure of Interests: None declared.

© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.