NSU Research Contributions
Title : CD98hc regulates the development of experimental colitis by controlling effector and regulatory CD4(+) T cells
Authors : Zaied Ahmed Bhuyan, Hideki Arimochi, Jun Nishida, Kataoka K, Kurihara T, Ishifune C, Hideki Tsumura, Morihiro Ito , Yasuhiko Ito, Akiko Kitamura, Koji Yasutomo
Abstract : 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.
| Journal : Biochem Biophys Res Commun | Volume : | Year : 2014 | Issue : 444(4) |
| Pages : 628-33 | City : | Edition : | Editors : |
| Publisher : | ISBN : | Book : | Chapter : |
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