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

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.

Pubmed ID: 20190759


  • Berger M
  • Krebs P
  • Crozat K
  • Li X
  • Croker BA
  • Siggs OM
  • Popkin D
  • Du X
  • Lawson BR
  • Theofilopoulos AN
  • Xia Y
  • Khovananth K
  • Moresco EM
  • Satoh T
  • Takeuchi O
  • Akira S
  • Beutler B


Nature immunology

Publication Data

April 19, 2010

Associated Grants

  • Agency: NIAID NIH HHS, Id: P01 AI070167
  • Agency: NIAID NIH HHS, Id: P01 AI070167-01
  • Agency: NIAID NIH HHS, Id: P01 AI070167-01
  • Agency: NIAID NIH HHS, Id: R01 AI076396
  • Agency: NIAMS NIH HHS, Id: R01 AR031203
  • Agency: NIGMS NIH HHS, Id: R37 GM067759

Mesh Terms

  • Animals
  • Apoptosis
  • Base Sequence
  • Cell Cycle Proteins
  • Cell Separation
  • Flow Cytometry
  • Immunologic Deficiency Syndromes
  • Leukocytes, Mononuclear
  • Lymphocyte Activation
  • Mice
  • Mice, Transgenic
  • Mutation
  • Phenotype
  • Signal Transduction
  • T-Lymphocytes