| First Author | Miller ML | Year | 2014 |
| Journal | Proc Natl Acad Sci U S A | Volume | 111 |
| Issue | 20 | Pages | 7397-402 |
| PubMed ID | 24799710 | Mgi Jnum | J:211053 |
| Mgi Id | MGI:5573076 | Doi | 10.1073/pnas.1315398111 |
| Citation | Miller ML, et al. (2014) Basal NF-kappaB controls IL-7 responsiveness of quiescent naive T cells. Proc Natl Acad Sci U S A 111(20):7397-402 |
| abstractText | T cells are essential for immune defenses against pathogens, such that viability of naive T cells before antigen encounter is critical to preserve a polyclonal repertoire and prevent immunodeficiencies. The viability of naive T cells before antigen recognition is ensured by IL-7, which drives expression of the prosurvival factor Bcl-2. Quiescent naive T cells have low basal activity of the transcription factor NF-kappaB, which was assumed to have no functional consequences. In contrast to this postulate, our data show that basal nuclear NF-kappaB activity plays an important role in the transcription of IL-7 receptor alpha-subunit (CD127), enabling responsiveness of naive T cells to the prosurvival effects of IL-7 and allowing T-cell persistence in vivo. Moreover, we show that this property of basal NF-kappaB activity is shared by mouse and human naive T cells. Thus, NF-kappaB drives a distinct transcriptional program in T cells before antigen encounter by controlling susceptibility to IL-7. Our results reveal an evolutionarily conserved role of NF-kappaB in T cells before antigenic stimulation and identify a novel molecular pathway that controls T-cell homeostasis. |
