A better understanding of the role of the CTLA–CD80/86 axis in the treatment of autoimmune diseases

Autoimmune diseases are diseases in which the regulatory mechanisms of the immune response are disturbed. As a result, the body loses self‐tolerance. Since one of the main regulatory mechanisms of the immune response is the CTLA4–CD80/86 axis, this hypothesis suggests that autoimmune diseases potent...

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Veröffentlicht in:Cell biochemistry and function 2024-01, Vol.42 (1), p.e3895-n/a
Hauptverfasser: Darvish, Zahra, Kheder, Ramiar Kamal, Faraj, Tola Abdulsattar, Najmaldin, Soran K., Mollazadeh, Samaneh, Nosratabadi, Reza, Esmaeili, Seyed‐Alireza
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Sprache:eng
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Zusammenfassung:Autoimmune diseases are diseases in which the regulatory mechanisms of the immune response are disturbed. As a result, the body loses self‐tolerance. Since one of the main regulatory mechanisms of the immune response is the CTLA4–CD80/86 axis, this hypothesis suggests that autoimmune diseases potentially share a similar molecular basis of pathogenesis. Hence, investigating the CTLA4–CD80/86 axis may be helpful in finding an appropriate treatment strategy. Therefore, this study aims to investigate the molecular basis of the CTLA4–CD80/86 axis in the regulation of the immune response, and then its role in developing some autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes, and multiple sclerosis. As well, the main therapeutic strategies affecting the CTLA4–CD80/86 axis have been summarized to highlight the importance of this axis in management of autoimmune diseases. Significance statement The CTLA4–CD80/86 axis as a major regulatory pathway in autoimmune diseases plays an important role in the pathogenesis of these diseases. Therefore, to find an appropriate treatment strategy, knowledge of the CTLA4–CD80/86 axis is helpful. Molecular basis and therapeutic strategies of the CTLA4–CD80/86 axis may help to treat autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes, and multiple sclerosis.
ISSN:0263-6484
1099-0844
DOI:10.1002/cbf.3895