• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

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

Authors

  • 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

Journal

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