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Nat Immunol. 2010 Apr;11(4):335-43. doi: 10.1038/ni.1847. Epub 2010 Feb 28.

An Slfn2 mutation causes lymphoid and myeloid immunodeficiency due to loss of immune cell quiescence.

Author information

1
Department of Genetics, The Scripps Research Institute, La Jolla, California, USA.

Abstract

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.

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PMID:
20190759
PMCID:
PMC2861894
DOI:
10.1038/ni.1847
[Indexed for MEDLINE]
Free PMC Article

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