| First Author | Bhuyan ZA | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 444 |
| Issue | 4 | Pages | 628-33 |
| PubMed ID | 24491544 | Mgi Jnum | J:219146 |
| Mgi Id | MGI:5619705 | Doi | 10.1016/j.bbrc.2014.01.144 |
| Citation | Bhuyan ZA, et al. (2014) CD98hc regulates the development of experimental colitis by controlling effector and regulatory CD4(+) T cells. Biochem Biophys Res Commun 444(4):628-33 |
| abstractText | CD4(+) T cell activation is controlled by signaling through the T cell receptor in addition to various co-receptors, and is also affected by their interactions with effector and regulatory T cells in the microenvironment. Inflammatory bowel diseases (IBD) are caused by the persistent activation and expansion of auto-aggressive CD4(+) T cells that attack intestinal epithelial cells. However, the molecular basis for the persistent activation of CD4(+) T cells in IBD remains unclear. In this study, we investigated how the CD98 heavy chain (CD98hc, Slc3a2) affected the development of colitis in an experimental animal model. Transferring CD98hc-deficient CD4(+)CD25(-) T cells into Rag2(-/-) mice did not cause colitis accompanied by increasing Foxp3(+) inducible regulatory T cells. By comparison, CD98hc-deficient naturally occurring regulatory T cells (nTregs) had a decreased capability to suppress colitis induced by CD4(+)CD25(-) T cells, although CD98hc-deficient mice did not have a defect in the development of nTregs. Blocking CD98hc with an anti-CD98 blocking antibody prevented the development of colitis. Our results indicate that CD98hc regulates the expansion of autoimmune CD4(+) T cells in addition to controlling nTregs functions, which suggests the CD98hc as an important target molecule for establishing strategies for treating colitis. |
