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Revista Paraguaya de Reumatología
versión On-line ISSN 2413-4341
Resumen
SERPA, Oscar Vicente Vergara et al. Role of IFN-λ in the pathogenesis of Systemic Lupus Erythematosus: biomolecular Mechanisms. Rev. parag. reumatol. [online]. 2024, vol.10, n.1, pp.37-45. Epub 27-Jun-2024. ISSN 2413-4341. https://doi.org/10.18004/rpr/2024.10.01.37.
Introduction:
Systemic lupus erythematosus (SLE) is an autoimmune disease that causes systemic inflammation and alterations in immunological tolerance. The activation of interferon (IFN)-inducible genes contributes to more than 50% of its pathogenesis. Objective: to review the role of IFN-λ in the pathogenesis of SLE. Materials and Methods: Systemic search in database; through the MeSH and DeCS keywords. The word “Lambda Interferon” was additionally included. Results: Aberrant production of type I interferon was found to contribute to the deregulation of IFN-λ, produced mainly by plasmacytoid dendritic cells. This process leads to immunological stimulation by autoantibodies and an increase in IFNλR-1 in B cells, enhancing the generation of antibodies. IFN-λ3 is particularly associated with lupus nephritis, and IFN-λ generally increases MHC-I expression, enhancing the CD8+ T cell response and possibly affecting central tolerance and regulation in the thymus. Conclusion: It is highlighted that IFN-λ favors immune activation, formation of immune complexes, chronic inflammation and production of autoantibodies, linking high levels of IFN-λ3 with greater disease activity.
Palabras clave : Autoimmunity; Interferons; Systemic lupus erythematosus; Interferon receptors; Toll-like receptors.