NDLI: Reduced lymphocyte longevity and homeostatic proliferation in lamin B receptor-deficient mice results in profound and progressive lymphopenia.

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Reduced lymphocyte longevity and homeostatic proliferation in lamin B receptor-deficient mice results in profound and progressive lymphopenia.

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Reduced lymphocyte longevity and homeostatic proliferation in lamin B receptor-deficient mice results in profound and progressive lymphopenia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hilton, Douglas J. Kile, Benjamin T. de Graaf, Carolyn A. Metcalf, Donald Verhagen, Anne M. Goradia, Ankita Collinge, Janelle E. Starr, Robyn Baldwin, Tracey M.
Description	Country affiliation: Australia Author Affiliation: Verhagen AM ( Walter and Eliza Hall Institute, Parkville, Victoria 3052, Australia. anne.verhagen@csl.com.au)
Abstract	The lamin B receptor (LBR) is a highly unusual inner nuclear membrane protein with multiple functions. Reduced levels are associated with decreased neutrophil lobularity, whereas complete absence of LBR results in severe skeletal dysplasia and in utero/perinatal lethality. We describe a mouse pedigree, Lym3, with normal bone marrow and thymic development but profound and progressive lymphopenia particularly within the T cell compartment. This defect arises from a point mutation within the Lbr gene with only trace mutant protein detectable in homozygotes, albeit sufficient for normal development. Reduced T cell homeostatic proliferative potential and life span in vivo were found to contribute to lymphopenia. To investigate the role of LBR in gene silencing in hematopoietic cells, we examined gene expression in wild-type and mutant lymph node CD8 T cells and bone marrow neutrophils. Although LBR deficiency had a very mild impact on gene expression overall, for common genes differentially expressed in both LBR-deficient CD8 T cells and neutrophils, gene upregulation prevailed, supporting a role for LBR in their suppression. In summary, this study demonstrates that LBR deficiency affects not only nuclear architecture but also proliferation, cell viability, and gene expression of hematopoietic cells.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	1
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Immunology Cell Aging Hematopoietic Stem Cells Lymphopenia Point Mutation Receptors, Cytoplasmic And Nuclear Animals Pathology Genetics Cell Proliferation Cell Survival Gene Expression Regulation Mice Mice, Knockout Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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