| CXCR4 and CCR5 expression delineates targets for HIV-1 disruption of T cell differentiation. | |
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MedLine Citation:
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PMID: 9759895 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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HIV-1 disease is often associated with CD4+ T lymphopenia as well as quantitative reductions in naive CD8+ T cells and cytopenias involving nonlymphoid hemopoietic lineages. Studies in HIV-1-infected humans as well as in animal models of lenti-virus disease indicate that these effects may be secondary to infection and destruction of multilineage and lineage-restricted hemopoietic progenitor cells. To define the stages of T cell differentiation that might be susceptible to HIV-1, we performed flow cytometric analysis of the surface expression of CXCR4 and CCR5 on T cells and their progenitors from fetal tissue, cord blood, SCID-hu Thy/Liv mice, and adult peripheral blood. We found that CXCR4 is expressed at low levels on hemopoietic progenitors in the bone marrow, is highly expressed on immature (CD3-CD4+CD8-) T cell progenitors in the thymus, and then is down-regulated during thymocyte differentiation. As thymocytes leave the thymus and enter the peripheral circulation, the expression of CXCR4 is again up-regulated. In contrast, CCR5 is undetectable on most hemopoietic progenitors in the bone marrow and on intrathymic T progenitor cells. It is up-regulated when thymocytes coexpress CD4 and CD8, then down-regulated either in the thymus (CD4+ cells) or during exit from the thymus (CD8+ cells). These results indicate that discrete, lineage-related populations of T cell progenitors may vary widely in their potential to respond to chemokines and to be infected by HIV-1, and that T lymphoid differentiation is particularly vulnerable to CXCR4-using viruses. |
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Authors:
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R D Berkowitz; K P Beckerman; T J Schall; J M McCune |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 161 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 1998 Oct |
Date Detail:
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Created Date: 1998-10-22 Completed Date: 1998-10-22 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 3702-10 Citation Subset: AIM; IM; X |
Affiliation:
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Gladstone Institute of Virology and Immunology, San Francisco, CA 94141-9100, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult Animals Bone Marrow Cells / metabolism Cell Differentiation / immunology Cells, Cultured Fetal Blood / cytology, metabolism HIV-1 / physiology* Humans Infant, Newborn Mice Mice, SCID Receptors, CCR5 / biosynthesis*, blood Receptors, CXCR4 / biosynthesis*, blood T-Lymphocyte Subsets / cytology, metabolism*, virology* Thymus Gland / cytology, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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R01-AI40312/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Receptors, CCR5; 0/Receptors, CXCR4 |
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