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Lrig1-expression confers suppressive function to CD4+ cells and is essential for averting autoimmunity via the Smad2/3/Foxp3 axis.
- Source :
- Nature Communications; 9/4/2023, Vol. 14 Issue 1, p1-16, 16p
- Publication Year :
- 2023
-
Abstract
- Regulatory T cells (T<subscript>reg</subscript>) are CD4<superscript>+</superscript> 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<superscript>+</superscript> T cells, T<subscript>reg</subscript> cells express the highest levels of Lrig1, and the expression level is further increasing with activation. The Lrig1<superscript>+</superscript> subpopulation from T helper (Th) 17 cells showed higher suppressive activity than the Lrig1<superscript>-</superscript> subpopulation. Lrig1-deficiency impairs the suppressive function of T<subscript>reg</subscript> cells, while Lrig1-deficient naïve T cells normally differentiate into other T cell subsets. Adoptive transfer of CD4<superscript>+</superscript>Lrig1<superscript>+</superscript> 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. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 20411723
- Volume :
- 14
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Nature Communications
- Publication Type :
- Academic Journal
- Accession number :
- 171364986
- Full Text :
- https://doi.org/10.1038/s41467-023-40986-4