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Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system
Rheumatoid arthritis and systemic lupus erythematosus are two highly prevalent autoimmune diseases that generate disability and low quality of life. The innate immune system, a long-forgotten issue in autoimmune diseases, is becoming increasingly important and represents a new focus for the treatmen...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8826259/ https://www.ncbi.nlm.nih.gov/pubmed/35154753 http://dx.doi.org/10.1177/2050312119876146 |
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author | Pabón-Porras, Maria Angélica Molina-Ríos, Sebastian Flórez-Suárez, Jorge Bruce Coral-Alvarado, Paola Ximena Méndez-Patarroyo, Paul Quintana-López, Gerardo |
author_facet | Pabón-Porras, Maria Angélica Molina-Ríos, Sebastian Flórez-Suárez, Jorge Bruce Coral-Alvarado, Paola Ximena Méndez-Patarroyo, Paul Quintana-López, Gerardo |
author_sort | Pabón-Porras, Maria Angélica |
collection | PubMed |
description | Rheumatoid arthritis and systemic lupus erythematosus are two highly prevalent autoimmune diseases that generate disability and low quality of life. The innate immune system, a long-forgotten issue in autoimmune diseases, is becoming increasingly important and represents a new focus for the treatment of these entities. This review highlights the role that innate immune system plays in the pathophysiology of rheumatoid arthritis and systemic lupus erythematosus. The role of the innate immune system in rheumatoid arthritis and systemic lupus erythematosus pathophysiology is not only important in early stages but is essential to maintain the immune response and to allow disease progression. In rheumatoid arthritis, genetic and environmental factors are involved in the initial stimulation of the innate immune response in which macrophages are the main participants, as well as fibroblast-like synoviocytes. In systemic lupus erythematosus, all the cells contribute to the inflammatory response, but the complement system is the major effector of the inflammatory process. Detecting alterations in the normal function of these cells, besides its contribution to the understanding of the pathophysiology of autoimmune diseases, could help to establish new treatment strategies for these diseases. |
format | Online Article Text |
id | pubmed-8826259 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-88262592022-02-10 Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system Pabón-Porras, Maria Angélica Molina-Ríos, Sebastian Flórez-Suárez, Jorge Bruce Coral-Alvarado, Paola Ximena Méndez-Patarroyo, Paul Quintana-López, Gerardo SAGE Open Med Review Paper Rheumatoid arthritis and systemic lupus erythematosus are two highly prevalent autoimmune diseases that generate disability and low quality of life. The innate immune system, a long-forgotten issue in autoimmune diseases, is becoming increasingly important and represents a new focus for the treatment of these entities. This review highlights the role that innate immune system plays in the pathophysiology of rheumatoid arthritis and systemic lupus erythematosus. The role of the innate immune system in rheumatoid arthritis and systemic lupus erythematosus pathophysiology is not only important in early stages but is essential to maintain the immune response and to allow disease progression. In rheumatoid arthritis, genetic and environmental factors are involved in the initial stimulation of the innate immune response in which macrophages are the main participants, as well as fibroblast-like synoviocytes. In systemic lupus erythematosus, all the cells contribute to the inflammatory response, but the complement system is the major effector of the inflammatory process. Detecting alterations in the normal function of these cells, besides its contribution to the understanding of the pathophysiology of autoimmune diseases, could help to establish new treatment strategies for these diseases. SAGE Publications 2019-09-13 /pmc/articles/PMC8826259/ /pubmed/35154753 http://dx.doi.org/10.1177/2050312119876146 Text en © The Author(s) 2019 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Review Paper Pabón-Porras, Maria Angélica Molina-Ríos, Sebastian Flórez-Suárez, Jorge Bruce Coral-Alvarado, Paola Ximena Méndez-Patarroyo, Paul Quintana-López, Gerardo Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system |
title | Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system |
title_full | Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system |
title_fullStr | Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system |
title_full_unstemmed | Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system |
title_short | Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system |
title_sort | rheumatoid arthritis and systemic lupus erythematosus: pathophysiological mechanisms related to innate immune system |
topic | Review Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8826259/ https://www.ncbi.nlm.nih.gov/pubmed/35154753 http://dx.doi.org/10.1177/2050312119876146 |
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