| First Author | Berger M | Year | 2010 |
| Journal | Nat Immunol | Volume | 11 |
| Issue | 4 | Pages | 335-43 |
| PubMed ID | 20190759 | Mgi Jnum | J:158985 |
| Mgi Id | MGI:4441014 | Doi | 10.1038/ni.1847 |
| Citation | Berger M, et al. (2010) An Slfn2 mutation causes lymphoid and myeloid immunodeficiency due to loss of immune cell quiescence. Nat Immunol 11(4):335-43 |
| abstractText | Here we describe a previously unknown form of inherited immunodeficiency revealed by an N-ethyl-N-nitrosourea-induced mutation called elektra. Mice homozygous for this mutation showed enhanced susceptibility to bacterial and viral infection and diminished numbers of T cells and inflammatory monocytes that failed to proliferate after infection and died via the intrinsic apoptotic pathway in response to diverse proliferative stimuli. They also had a greater proportion of T cells poised to replicate DNA, and their T cells expressed a subset of activation markers, suggestive of a semi-activated state. We positionally ascribe the elektra phenotype to a mutation in the gene encoding Schlafen-2 (Slfn2). Our findings identify a physiological role for Slfn2 in the defense against pathogens through the regulation of quiescence in T cells and monocytes. |
