| Getting back at nature: understanding thymic development and overcoming its atrophy. | |
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MedLine Citation:
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PMID: 20483662 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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T cell development is a complex and tightly regulated process involving reciprocal interactions between the thymic stroma and differentiating thymocytes. Normal thymic function is critical for immunity and microenvironmental defects predispose to dysregulation in the T cell compartment. Thymic structure and function are also severely damaged by chemotherapy and pre-transplant conditioning. Furthermore, poor immune competence with ageing is closely linked to thymic atrophy. Overcoming such thymic defects would have immediate application in many diseases, especially the recovery of cancer patients from cytotoxic treatment. Reversing the thymus ageing process via inhibition of atrophic factors such as sex steroids or administration of thymopoietic growth factors is one possible approach. Moreover, it is becoming clear a common thymic epithelial progenitor exists, raising the possibility for de novo thymus generation using emerging stem cell and tissue engineering technologies. Achievement of this goal will open up many avenues for the application of thymus-based immune rejuvenation and manipulation. |
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Authors:
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Tracy S P Heng; Ann P Chidgey; Richard L Boyd |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2010-05-17 |
Journal Detail:
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Title: Current opinion in pharmacology Volume: 10 ISSN: 1471-4973 ISO Abbreviation: Curr Opin Pharmacol Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-08-03 Completed Date: 2010-11-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100966133 Medline TA: Curr Opin Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 425-33 Citation Subset: IM |
Copyright Information:
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Copyright 2010 Elsevier Ltd. All rights reserved. |
Affiliation:
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Monash Immunology and Stem Cell Laboratories, Monash University, Clayton, VIC 3800, Australia. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aging
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immunology,
physiology* Animals Antineoplastic Agents / toxicity Atrophy / chemically induced Epithelial Cells Fibroblast Growth Factor 7 / pharmacology Gonadal Steroid Hormones / antagonists & inhibitors Growth Hormone / pharmacology Humans Insulin-Like Growth Factor I / pharmacology Interleukin-7 / pharmacology Membrane Proteins / pharmacology Stem Cells / physiology Stromal Cells T-Lymphocytes / drug effects, immunology, physiology* Thymus Gland / drug effects, immunology, physiology* fms-Like Tyrosine Kinase 3 / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Antineoplastic Agents; 0/Gonadal Steroid Hormones; 0/Interleukin-7; 0/Membrane Proteins; 0/flt3 ligand protein; 126469-10-1/Fibroblast Growth Factor 7; 67763-96-6/Insulin-Like Growth Factor I; 9002-72-6/Growth Hormone; EC 2.7.10.1/FLT3 protein, human; EC 2.7.10.1/fms-Like Tyrosine Kinase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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