2005/12/22 by Christian Dejaco, Christina Duftner, Beatrix Grubeck‐Loebenstein +1
Immunology and Microbiology · #IL-33, ST2, and ILC Pathways #Immune Cell Function and Interaction #T-cell and B-cell Immunology
paper · doi:10.1111/j.1365-2567.2005.02317.x
openalex publication_date 2005/12/22 · crossref created 2005/12/22 · crossref issued 2006/02/13 · crossref published 2006/02/13 · crossref published-online 2006/02/13 · crossref published-print 2006/03/01 · crossref deposited 2023/10/13 · openalex created_date 2025/10/10 · crossref indexed 2026/07/29 · openalex updated_date 2026/07/30
The breakdown of mechanisms assuring the recognition of self and non-self is a hallmark feature of autoimmune diseases. In the past 10 years, there has been a steadily increasing interest in a subpopulation of regulatory T cells, which exert their suppressive function in vitro in a contact-dependent manner and preferentially express high levels of CD25 and forkhead and winged-helix family transcription factor forkhead box P3 (FOXP3) (TREGs). Recent findings of changed prevalences and functional efficiencies indicate that these TREGs play a unique role in autoimmune diseases. Clinical findings in patients with mutated FOXP3 genes and a specific polymorphism in the promotor region of FOXP3 also support the role of FOXP3 as a 'master control gene' in the development and functioning of TREGs. Both altered generation of TREGs and insufficient suppression of inflammation in autoimmune diseases are considered to be crucial for the initiation and perpetuation of disease. TREG-related somatic cell therapy is considered as an intriguing new intervention to approach autoimmune diseases.