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Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside

Systemic lupus erythematosus (SLE) is considered an autoimmune disease with multiorgan involvement. Many advances have been made during the last decade regarding inflammatory pathways, genetic and epigenetic alterations, adaptive and innate immune system mechanisms specifically involved in SLE patho...

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Detalles Bibliográficos
Autores principales: Squatrito, D., Emmi, G., Silvestri, E., Ciucciarelli, L., D’Elios, M. M., Prisco, D., Emmi, L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389042/
https://www.ncbi.nlm.nih.gov/pubmed/26000154
http://dx.doi.org/10.1007/s13317-014-0058-y
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author Squatrito, D.
Emmi, G.
Silvestri, E.
Ciucciarelli, L.
D’Elios, M. M.
Prisco, D.
Emmi, L.
author_facet Squatrito, D.
Emmi, G.
Silvestri, E.
Ciucciarelli, L.
D’Elios, M. M.
Prisco, D.
Emmi, L.
author_sort Squatrito, D.
collection PubMed
description Systemic lupus erythematosus (SLE) is considered an autoimmune disease with multiorgan involvement. Many advances have been made during the last decade regarding inflammatory pathways, genetic and epigenetic alterations, adaptive and innate immune system mechanisms specifically involved in SLE pathogenesis. Apoptosis has been proposed as an important player in SLE pathogenesis more than a decade ago. However, only recently new key apoptotic pathways have been investigated and the link between apoptotic debris containing autoantigens, innate immunity and ongoing inflammation has been further elucidated. Better understanding of cellular mechanisms and involved cytokines contributed to the development of new biological drugs specifically addressed for SLE therapy.
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spelling pubmed-43890422015-05-21 Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside Squatrito, D. Emmi, G. Silvestri, E. Ciucciarelli, L. D’Elios, M. M. Prisco, D. Emmi, L. Auto Immun Highlights Review Article Systemic lupus erythematosus (SLE) is considered an autoimmune disease with multiorgan involvement. Many advances have been made during the last decade regarding inflammatory pathways, genetic and epigenetic alterations, adaptive and innate immune system mechanisms specifically involved in SLE pathogenesis. Apoptosis has been proposed as an important player in SLE pathogenesis more than a decade ago. However, only recently new key apoptotic pathways have been investigated and the link between apoptotic debris containing autoantigens, innate immunity and ongoing inflammation has been further elucidated. Better understanding of cellular mechanisms and involved cytokines contributed to the development of new biological drugs specifically addressed for SLE therapy. Springer International Publishing 2014-08-14 /pmc/articles/PMC4389042/ /pubmed/26000154 http://dx.doi.org/10.1007/s13317-014-0058-y Text en © Springer International Publishing Switzerland 2014
spellingShingle Review Article
Squatrito, D.
Emmi, G.
Silvestri, E.
Ciucciarelli, L.
D’Elios, M. M.
Prisco, D.
Emmi, L.
Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside
title Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside
title_full Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside
title_fullStr Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside
title_full_unstemmed Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside
title_short Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside
title_sort pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389042/
https://www.ncbi.nlm.nih.gov/pubmed/26000154
http://dx.doi.org/10.1007/s13317-014-0058-y
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