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Department of Pathology and Laboratory Medicine and the Jonsson Comprehensive Cancer Center (E.M.-R., K.D.), University of California, Los Angeles School of Medicine, Los Angeles, California 90025-1732; and the Research Center for Developmental Medicine and Biology (R.C.), Faculty of Medicine and Health Sciences, University of Auckland, Auckland, New Zealand
Address all correspondence and requests for reprints to: Dr. Kenneth Dorshkind, Department of Pathology 173216, University of California, Los Angeles School of Medicine, 10833 Le Conte Avenue, Los Angeles, California 90095-1732. E-mail: kdorshki{at}pathology.medsch.ucla.edu
There has been considerable interest in using hormone replacement therapy to rejuvenate the involuted thymus during aging. GH and insulin-like growth factor-I (IGF-I), a mediator of GH actions, have been of particular interest because of their thymopoietic effects and the fact that their serum concentrations decline during aging. However, treatment of aging rodents with either GH or IGF-I does not restore thymus cellularity to levels present in young animals, suggesting that additional defects might limit the magnitude of their effects. In particular, deficiencies have been reported to accumulate in the bone marrow T cell precursor compartment during aging. In view of this, 18-month-old mice were administered either recombinant IGF-I, bone marrow cells from young mice, or a combination of IGF-I and young bone marrow cells. Thymus cellularity in the latter group of mice was significantly higher than in animals treated with hormone or bone marrow transplantation alone, suggesting that optimal therapies for restoring thymus cellularity must address both endocrine and hematopoietic defects that accumulate during aging. Results from in vitro studies using fetal thymic organ cultures suggest that IGF-I acts by potentiating thymic colonization by bone marrow T cell precursors and/or that the hormone affects some other event soon after thymus colonization.
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