| First Author | Notake T | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 10 | Pages | 4838-45 |
| PubMed ID | 22504642 | Mgi Jnum | J:188674 |
| Mgi Id | MGI:5441419 | Doi | 10.4049/jimmunol.1200210 |
| Citation | Notake T, et al. (2012) Differential requirements for IRF-2 in generation of CD1d-independent T cells bearing NK cell receptors. J Immunol 188(10):4838-45 |
| abstractText | NK cell receptors (NKRs) such as NK1.1, NKG2D, and Ly49s are expressed on subsets of CD1d-independent memory phenotype CD8(+) and CD4(-)CD8(-) T cells. However, the mechanism for the generation and functions of these NKR(+) T cells remained elusive. In this study, we found that CD1d-independent Ly49(+) T cells were reduced severely in the spleen, bone marrow, and liver, but not thymus, in mice doubly deficient for IFN regulatory factor-2 (IRF-2) and CD1d, in which the overall memory phenotype T cell population was contrastingly enlarged. Because a large fraction of Ly49(+) T cells coexpressed NK1.1 or NKG2D, the reduction of Ly49(+) T cells resulted indirectly in underrepresentation of NK1.1(+) or NKG2D(+) cells. Ly49(+) T cell deficiency was observed in IRF-2(-/-) mice additionally lacking IFN-alpha/betaR alpha-chain (IFNAR1) as severely as in IRF-2(-/-) mice, arguing against the involvement of the accelerated IFN-alpha/beta signals due to IRF-2 deficiency. Rather, mice lacking IFN-alpha/betaR alone also exhibited relatively milder Ly49(+) T cell reduction, and IL-2 could expand Ly49(+) T cells from IFNAR1(-/-), but not from IRF-2(-/-), spleen cells in vitro. These results together indicated that IRF-2 acted in Ly49(+) T cell development in a manner distinct from that of IFN-alpha/beta signals. The influence of IRF-2 deficiency on Ly49(+) memory phenotype T cells observed in this study suggested a unique transcriptional program for this T cell population among other NKR(+) T and memory phenotype T cells. |
