期刊
NATURE IMMUNOLOGY
卷 11, 期 4, 页码 335-U55出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1847
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- NIAID NIH HHS [P01 AI070167, R01 AI076396, P01 AI070167-01] Funding Source: Medline
- NIAMS NIH HHS [R01 AR031203] Funding Source: Medline
- NIGMS NIH HHS [R37 GM067759] Funding Source: Medline
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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