| First Author | Lian G | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 5 | Pages | 2227-34 |
| PubMed ID | 22291182 | Mgi Jnum | J:181360 |
| Mgi Id | MGI:5311084 | Doi | 10.4049/jimmunol.1102586 |
| Citation | Lian G, et al. (2012) Manipulation of CD98 Resolves Type 1 Diabetes in Nonobese Diabetic Mice. J Immunol 188(5):2227-34 |
| abstractText | The interplay of CD4(+) and CD8(+) T cells targeting autoantigens is responsible for the progression of a number of autoimmune diseases, including type 1 diabetes mellitus (T1D). Understanding the molecular mechanisms that regulate T cell activation is crucial for designing effective therapies for autoimmune diseases. We probed a panel of Abs with T cell-modulating activity and identified a mAb specific for the H chain of CD98 (CD98hc) that was able to suppress T cell proliferation. The anti-CD98hc mAb also inhibited Ag-specific proliferation and the acquisition of effector function by CD4(+) and CD8(+) T cells in vitro and in vivo. Injection of the anti-CD98hc mAb completely prevented the onset of cyclophosphamide-induced diabetes in NOD mice. Treatment of diabetic NOD mice with anti-CD98hc reversed the diabetic state to normal levels, coincident with decreased proliferation of CD4(+) T cells. Furthermore, treatment of diabetic NOD mice with CD98hc small interfering RNA resolved T1D. These data indicate that strategies targeting CD98hc might have clinical application for treating T1D and other T cell-mediated autoimmune diseases. |
