The Role of the Oxidative State and Innate Immunity Mediated by TLR7 and TLR9 in Lupus Nephritis
Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE) and is considered one of the leading causes of mortality. Multiple immunological pathways are involved in the pathogenesis of SLE, which makes it imperative to deepen our knowledge about this disease's immune-pa...
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creator | Echavarria, Raquel Cardona-Muñoz, Ernesto Germán Ortiz-Lazareno, Pablo Andrade-Sierra, Jorge Gómez-Hermosillo, Luis Francisco Casillas-Moreno, Jorge Campos-Bayardo, Tannia Isabel Román-Rojas, Daniel García-Sánchez, Andrés Miranda-Díaz, Alejandra Guillermina |
description | Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE) and is considered one of the leading causes of mortality. Multiple immunological pathways are involved in the pathogenesis of SLE, which makes it imperative to deepen our knowledge about this disease's immune-pathological complexity and explore new therapeutic targets. Since an altered redox state contributes to immune system dysregulation, this document briefly addresses the roles of oxidative stress (OS), oxidative DNA damage, antioxidant enzymes, mitochondrial function, and mitophagy in SLE and LN. Although adaptive immunity's participation in the development of autoimmunity is undeniable, increasing data emphasize the importance of innate immunity elements, particularly the Toll-like receptors (TLRs) that recognize nucleic acid ligands, in inflammatory and autoimmune diseases. Here, we discuss the intriguing roles of TLR7 and TLR9 in developing SLE and LN. Also included are the essential characteristics of conventional treatments and some other novel and little-explored alternatives that offer options to improve renal function in LN. |
doi_str_mv | 10.3390/ijms242015234 |
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Multiple immunological pathways are involved in the pathogenesis of SLE, which makes it imperative to deepen our knowledge about this disease's immune-pathological complexity and explore new therapeutic targets. Since an altered redox state contributes to immune system dysregulation, this document briefly addresses the roles of oxidative stress (OS), oxidative DNA damage, antioxidant enzymes, mitochondrial function, and mitophagy in SLE and LN. Although adaptive immunity's participation in the development of autoimmunity is undeniable, increasing data emphasize the importance of innate immunity elements, particularly the Toll-like receptors (TLRs) that recognize nucleic acid ligands, in inflammatory and autoimmune diseases. Here, we discuss the intriguing roles of TLR7 and TLR9 in developing SLE and LN. Also included are the essential characteristics of conventional treatments and some other novel and little-explored alternatives that offer options to improve renal function in LN.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms242015234</identifier><identifier>PMID: 37894915</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Aldehydes ; Antigens ; Antioxidants ; Atherosclerosis ; Autoimmune diseases ; Autoimmunity ; B cells ; Blood coagulation factors ; Carotenoids ; Dehydrogenases ; Development and progression ; Dietary minerals ; Disease ; DNA damage ; Enzymes ; Flavonoids ; Humans ; Immunity, Innate ; Inflammation ; Lipids ; Lupus ; Lupus Erythematosus, Systemic ; Lupus Nephritis - metabolism ; Metabolites ; Mitochondria ; Mortality ; Nephritis ; Neutrophils ; Nitric oxide ; Nucleic acids ; Oxidation ; Oxidation-Reduction ; Oxidative stress ; Pathogenesis ; Proteins ; Review ; Systemic lupus erythematosus ; Thrombosis ; Toll-Like Receptor 7 - genetics ; Toll-Like Receptor 9 - metabolism ; Uric acid</subject><ispartof>International journal of molecular sciences, 2023-10, Vol.24 (20), p.15234</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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Multiple immunological pathways are involved in the pathogenesis of SLE, which makes it imperative to deepen our knowledge about this disease's immune-pathological complexity and explore new therapeutic targets. Since an altered redox state contributes to immune system dysregulation, this document briefly addresses the roles of oxidative stress (OS), oxidative DNA damage, antioxidant enzymes, mitochondrial function, and mitophagy in SLE and LN. Although adaptive immunity's participation in the development of autoimmunity is undeniable, increasing data emphasize the importance of innate immunity elements, particularly the Toll-like receptors (TLRs) that recognize nucleic acid ligands, in inflammatory and autoimmune diseases. Here, we discuss the intriguing roles of TLR7 and TLR9 in developing SLE and LN. Also included are the essential characteristics of conventional treatments and some other novel and little-explored alternatives that offer options to improve renal function in LN.</description><subject>Aldehydes</subject><subject>Antigens</subject><subject>Antioxidants</subject><subject>Atherosclerosis</subject><subject>Autoimmune diseases</subject><subject>Autoimmunity</subject><subject>B cells</subject><subject>Blood coagulation factors</subject><subject>Carotenoids</subject><subject>Dehydrogenases</subject><subject>Development and progression</subject><subject>Dietary minerals</subject><subject>Disease</subject><subject>DNA damage</subject><subject>Enzymes</subject><subject>Flavonoids</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Inflammation</subject><subject>Lipids</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic</subject><subject>Lupus Nephritis - metabolism</subject><subject>Metabolites</subject><subject>Mitochondria</subject><subject>Mortality</subject><subject>Nephritis</subject><subject>Neutrophils</subject><subject>Nitric oxide</subject><subject>Nucleic acids</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Review</subject><subject>Systemic lupus erythematosus</subject><subject>Thrombosis</subject><subject>Toll-Like Receptor 7 - 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Multiple immunological pathways are involved in the pathogenesis of SLE, which makes it imperative to deepen our knowledge about this disease's immune-pathological complexity and explore new therapeutic targets. Since an altered redox state contributes to immune system dysregulation, this document briefly addresses the roles of oxidative stress (OS), oxidative DNA damage, antioxidant enzymes, mitochondrial function, and mitophagy in SLE and LN. Although adaptive immunity's participation in the development of autoimmunity is undeniable, increasing data emphasize the importance of innate immunity elements, particularly the Toll-like receptors (TLRs) that recognize nucleic acid ligands, in inflammatory and autoimmune diseases. Here, we discuss the intriguing roles of TLR7 and TLR9 in developing SLE and LN. 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subjects | Aldehydes Antigens Antioxidants Atherosclerosis Autoimmune diseases Autoimmunity B cells Blood coagulation factors Carotenoids Dehydrogenases Development and progression Dietary minerals Disease DNA damage Enzymes Flavonoids Humans Immunity, Innate Inflammation Lipids Lupus Lupus Erythematosus, Systemic Lupus Nephritis - metabolism Metabolites Mitochondria Mortality Nephritis Neutrophils Nitric oxide Nucleic acids Oxidation Oxidation-Reduction Oxidative stress Pathogenesis Proteins Review Systemic lupus erythematosus Thrombosis Toll-Like Receptor 7 - genetics Toll-Like Receptor 9 - metabolism Uric acid |
title | The Role of the Oxidative State and Innate Immunity Mediated by TLR7 and TLR9 in Lupus Nephritis |
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