Document Detail


Distinct patterns of Fas cell surface expression during development of T- or B-lymphocyte lineages in normal, scid, and mutant mice lacking or overexpressing p53, bcl-2, or rag-2 genes.
MedLine Citation:
PMID:  8788039     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fas is a cell membrane protein involved in programmed cell death. In normal young mice, Fas was expressed on pluripotent stem cells, multipotent progenitors, pro-T and pre-T cells, most thymocytes, and a subset of CD4 and CD8 mature T lymphocytes. In contrast, Fas expression was switched off in B-cell and myelocytic progenitors and most pro-B and a proportion of pre-B cells and was switched on again later, but this occurred only in a subset of mature B lymphocytes. A lack of bcl-2 increased the proportion of Fas+ B-lymphocyte lineage cells and Fas+ CD4+ cells and decreased the percentage of Fas- CD8+ mature T-cell subsets. Overexpression of bcl-2 reversed this pattern of Fas cell surface expression. Interestingly, lack of p53 increased the proportions of Fas-expressing CD4 and CD8 mature T-cell subsets and of Fas- B-cell precursors but decreased that of Fas- mature B-lymphocyte populations. We conclude that the expression of Fas is regulated distinctly during the development of T and B lymphocytes. Although the products of neither bcl-2 nor p53 genes are essential for Fas cell surface expression on hematopoietic cells, these repressor and effector genes, respectively, of programmed cell death affect distinct subsets of lymphoid lineage cells at different stages of lymphopoiesis. Our results suggest that distinct combinations of effector and suppressor genes of programmed cell death act on distinct cell populations and at different stages of differentiation within the same cell lineage in the hematopoietic system.
Authors:
T Li; K Ramirez; R Palacios
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research     Volume:  7     ISSN:  1044-9523     ISO Abbreviation:  Cell Growth Differ.     Publication Date:  1996 Jan 
Date Detail:
Created Date:  1996-10-31     Completed Date:  1996-10-31     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9100024     Medline TA:  Cell Growth Differ     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  107-14     Citation Subset:  IM    
Affiliation:
Department of Immunology, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD95 / genetics*
Apoptosis / genetics,  immunology
B-Lymphocytes / cytology,  physiology
Biological Markers
Cell Differentiation / immunology
DNA-Binding Proteins*
Erythroid Precursor Cells / cytology,  immunology,  physiology
Female
Flow Cytometry
Gene Expression / immunology
Genes, bcl-2 / genetics*,  immunology
Genes, p53 / immunology*
Male
Membrane Proteins / genetics
Mice
Mice, Mutant Strains
Mice, SCID
Mice, Transgenic
Protein-Tyrosine Kinases / genetics*,  immunology
Proteins / genetics*,  immunology
T-Lymphocytes / cytology,  physiology
Transgenes / immunology
Grant Support
ID/Acronym/Agency:
CA-16672-18/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD95; 0/Biological Markers; 0/DNA-Binding Proteins; 0/Membrane Proteins; 0/Proteins; 0/Rag2 protein, mouse; 0/V(D)J recombination activating protein 2; EC 2.7.10.1/Protein-Tyrosine Kinases

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