| First Author | MaruYama T | Year | 2015 |
| Journal | J Leukoc Biol | Volume | 98 |
| Issue | 3 | Pages | 385-93 |
| PubMed ID | 26019294 | Mgi Jnum | J:242738 |
| Mgi Id | MGI:5906114 | Doi | 10.1189/jlb.2A0814-384R |
| Citation | MaruYama T, et al. (2015) Control of IFN-gamma production and regulatory function by the inducible nuclear protein IkappaB-zeta in T cells. J Leukoc Biol 98(3):385-93 |
| abstractText | The transcriptional regulator IkappaB-zeta is important for the control of apoptosis in keratinocytes. Thus, IkappaB-zeta-deficient mice develop autoimmune diseases, such as Sjogren's syndrome. However, T cells also play a pivotal role in Sjogren's syndrome. To study the role of IkappaB-zeta in T cells, we generated T cell-specific, IkappaB-zeta-deficient mice. We observed increased numbers of peripheral effector/memory CD4(+) cells and IFN-gamma-producing CD4(+) cells in 3-week-old mice. We found that IkappaB-zeta can be up-regulated by TGF-beta1 in naive CD4(+) T cells and that it negatively regulates IFN-gamma expression. In addition, we generated Treg-specific, IkappaB-zeta deficient mice and found that IkappaB-zeta is dispensable for the plasticity and stability of Tregs. However, Tregs from T cell-specific, IkappaB-zeta-deficient mice have reduced immunoregulatory function. Thus, our data reveal a previously unappreciated role for IkappaB-zeta in IFN-gamma production in T cells and the immunoregulatory function of Tregs. |
