| First Author | Moon JS | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 5382 |
| PubMed ID | 37666819 | Mgi Jnum | J:339871 |
| Mgi Id | MGI:7524486 | Doi | 10.1038/s41467-023-40986-4 |
| Citation | Moon JS, et al. (2023) Lrig1-expression confers suppressive function to CD4(+) cells and is essential for averting autoimmunity via the Smad2/3/Foxp3 axis. Nat Commun 14(1):5382 |
| abstractText | Regulatory T cells (T(reg)) 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, T(reg) 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 T(reg) cells, while Lrig1-deficient naive 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. |
