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

  • Published In: Cell Biochemistry & Function, 2024, v. 42, n. 1. P. 1 1 of 3

  • Database: Academic Search Ultimate 2 of 3

  • Authored By: Darvish, Zahra; Kheder, Ramiar Kamal; Faraj, Tola Abdulsattar; Najmaldin, Soran K.; Mollazadeh, Samaneh; Nosratabadi, Reza; Esmaeili, Seyed‐Alireza 3 of 3

Abstract

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. [ABSTRACT FROM AUTHOR]

Additional Information

  • Source:Cell Biochemistry & Function. 2024/01, Vol. 42, Issue 1, p1
  • Document Type:Article
  • Subject Area:Complementary and Alternative Medicine
  • Publication Date:2024
  • ISSN:0263-6484
  • DOI:10.1002/cbf.3895
  • Accession Number:175056802
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