Rheumatoid Arthritis: What Inflammation Do We Face?
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by symmetrical joint inflammation, cartilage degradation, and bone erosion. This review explores the multifaceted aspects of RA pathogenesis, focusing on the dynamic interplay between innate and adaptive immune responses, geneti...
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| Format: | Article |
| Language: | English |
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MDPI AG
2024-10-01
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| Series: | Journal of Molecular Pathology |
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| author | Anastasia V. Poznyak Tatyana Vladimirovna Kirichenko Dmitry Felixovich Beloyartsev Alexey V. Churov Tatiana Ivanovna Kovyanova Irina Alexandrovna Starodubtseva Vasily N. Sukhorukov Stanislav A. Antonov Alexander N. Orekhov |
| author_facet | Anastasia V. Poznyak Tatyana Vladimirovna Kirichenko Dmitry Felixovich Beloyartsev Alexey V. Churov Tatiana Ivanovna Kovyanova Irina Alexandrovna Starodubtseva Vasily N. Sukhorukov Stanislav A. Antonov Alexander N. Orekhov |
| author_sort | Anastasia V. Poznyak |
| collection | DOAJ |
| description | Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by symmetrical joint inflammation, cartilage degradation, and bone erosion. This review explores the multifaceted aspects of RA pathogenesis, focusing on the dynamic interplay between innate and adaptive immune responses, genetic predisposition, and environmental triggers. The development of RA involves genetic susceptibility and trigger events such as infections, trauma, smoking, obesity, and microbiome alterations, fostering autoimmune reactions and tissue/organ destruction. The innate immune response, including toll-like receptor activation and synovial fibroblasts’ roles, contributes to the acceleration of inflammatory processes in joint tissues. Monocytes and macrophages organize and sustain chronic joint inflammation, leading to tissue damage and bone resorption, while highlighting the significance of CD14 and CD16 subsets in RA pathogenesis. In the adaptive immune response, aberrant activation and proliferation of CD4+ T cells and the role of regulatory T cells in maintaining immune tolerance are discussed. Target cytokines like TNF-α, IL-6, IL-1, IL-17, and BAFF, as well as chemokines such as CCL2, CXCL10, CCL5, and CXCL12, have emerged as critical components in managing chronic inflammation and joint damage in RA. This comprehensive overview provides insights into the pathophysiology of RA and potential therapeutic avenues, emphasizing the importance of understanding these complex immunological and genetic mechanisms for developing more effective treatment strategies. |
| format | Article |
| id | doaj-art-73e57f6643d64d1b983ff6db717df708 |
| institution | DOAJ |
| issn | 2673-5261 |
| language | English |
| publishDate | 2024-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Journal of Molecular Pathology |
| spelling | doaj-art-73e57f6643d64d1b983ff6db717df7082025-08-20T02:50:59ZengMDPI AGJournal of Molecular Pathology2673-52612024-10-015445446510.3390/jmp5040030Rheumatoid Arthritis: What Inflammation Do We Face?Anastasia V. Poznyak0Tatyana Vladimirovna Kirichenko1Dmitry Felixovich Beloyartsev2Alexey V. Churov3Tatiana Ivanovna Kovyanova4Irina Alexandrovna Starodubtseva5Vasily N. Sukhorukov6Stanislav A. Antonov7Alexander N. Orekhov8Institute for Atherosclerosis Research, Osennyaya 4-1-207, 121609 Moscow, RussiaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 8 Baltiiskaya Street, 125315 Moscow, RussiaVascular Surgery Department, A. V. Vishnevsky National Medical Research Center of Surgery, 27 Bolshaya Serpukhovskaya Street, 117997 Moscow, RussiaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 8 Baltiiskaya Street, 125315 Moscow, RussiaInstitute for Atherosclerosis Research, Osennyaya 4-1-207, 121609 Moscow, RussiaDepartment of Polyclinic Therapy, NN Burdenko Voronezh State Medical University, 10 Studencheskaya Street, 394036 Voronezh, RussiaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 8 Baltiiskaya Street, 125315 Moscow, RussiaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 8 Baltiiskaya Street, 125315 Moscow, RussiaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 8 Baltiiskaya Street, 125315 Moscow, RussiaRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by symmetrical joint inflammation, cartilage degradation, and bone erosion. This review explores the multifaceted aspects of RA pathogenesis, focusing on the dynamic interplay between innate and adaptive immune responses, genetic predisposition, and environmental triggers. The development of RA involves genetic susceptibility and trigger events such as infections, trauma, smoking, obesity, and microbiome alterations, fostering autoimmune reactions and tissue/organ destruction. The innate immune response, including toll-like receptor activation and synovial fibroblasts’ roles, contributes to the acceleration of inflammatory processes in joint tissues. Monocytes and macrophages organize and sustain chronic joint inflammation, leading to tissue damage and bone resorption, while highlighting the significance of CD14 and CD16 subsets in RA pathogenesis. In the adaptive immune response, aberrant activation and proliferation of CD4+ T cells and the role of regulatory T cells in maintaining immune tolerance are discussed. Target cytokines like TNF-α, IL-6, IL-1, IL-17, and BAFF, as well as chemokines such as CCL2, CXCL10, CCL5, and CXCL12, have emerged as critical components in managing chronic inflammation and joint damage in RA. This comprehensive overview provides insights into the pathophysiology of RA and potential therapeutic avenues, emphasizing the importance of understanding these complex immunological and genetic mechanisms for developing more effective treatment strategies.https://www.mdpi.com/2673-5261/5/4/30rheumatoid arthritisinflammationautoimmune diseaseimmune responsecytokineschemokines |
| spellingShingle | Anastasia V. Poznyak Tatyana Vladimirovna Kirichenko Dmitry Felixovich Beloyartsev Alexey V. Churov Tatiana Ivanovna Kovyanova Irina Alexandrovna Starodubtseva Vasily N. Sukhorukov Stanislav A. Antonov Alexander N. Orekhov Rheumatoid Arthritis: What Inflammation Do We Face? Journal of Molecular Pathology rheumatoid arthritis inflammation autoimmune disease immune response cytokines chemokines |
| title | Rheumatoid Arthritis: What Inflammation Do We Face? |
| title_full | Rheumatoid Arthritis: What Inflammation Do We Face? |
| title_fullStr | Rheumatoid Arthritis: What Inflammation Do We Face? |
| title_full_unstemmed | Rheumatoid Arthritis: What Inflammation Do We Face? |
| title_short | Rheumatoid Arthritis: What Inflammation Do We Face? |
| title_sort | rheumatoid arthritis what inflammation do we face |
| topic | rheumatoid arthritis inflammation autoimmune disease immune response cytokines chemokines |
| url | https://www.mdpi.com/2673-5261/5/4/30 |
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