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- Title
Lrig1-expression confers suppressive function to CD4<sup>+</sup> cells and is essential for averting autoimmunity via the Smad2/3/Foxp3 axis.
- Authors
Moon, Jae-Seung; Ho, Chun-Chang; Park, Jong-Hyun; Park, Kyungsoo; Shin, Bo-Young; Lee, Su-Hyeon; Sequeira, Ines; Mun, Chin Hee; Shin, Jin-Su; Kim, Jung-Ho; Kim, Beom Seok; Noh, Jin-Wook; Lee, Eui-Seon; Son, Ji Young; Kim, Yuna; lee, Yeji; Cho, Hee; So, SunHyeon; Park, Jiyoon; Choi, Eunsu
- Abstract
Regulatory T cells (Treg) are CD4+ T cells with immune-suppressive function, which is defined by Foxp3 expression. However, the molecular determinants defining the suppressive population of T cells have yet to be discovered. Here we report that the cell surface protein Lrig1 is enriched in suppressive T cells and controls their suppressive behaviors. Within CD4+ T cells, Treg cells express the highest levels of Lrig1, and the expression level is further increasing with activation. The Lrig1+ subpopulation from T helper (Th) 17 cells showed higher suppressive activity than the Lrig1- subpopulation. Lrig1-deficiency impairs the suppressive function of Treg cells, while Lrig1-deficient naïve T cells normally differentiate into other T cell subsets. Adoptive transfer of CD4+Lrig1+ T cells alleviates autoimmune symptoms in colitis and lupus nephritis mouse models. A monoclonal anti-Lrig1 antibody significantly improves the symptoms of experimental autoimmune encephalomyelitis. In conclusion, Lrig1 is an important regulator of suppressive T cell function and an exploitable target for treating autoimmune conditions. Regulatory T cells, and to certain extent other T cell subsets, limit the immune response to avoid harmful inflammation and tissue damage. Here authors identify a surface molecule, Lrig1, that is directly responsible for the suppressive function in regulatory T cells and in Il-17-producing helper T cells.
- Subjects
REGULATORY T cells; T helper cells; CELL physiology; T cells; CELL populations; T cell receptors; AUTOIMMUNITY
- Publication
Nature Communications, 2023, Vol 14, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-023-40986-4