Growth Hormone and Immune Function in the Elderly

Over 20 years ago it was recognized that both the Ames and Snell-Bagg (DW/J) dwarf mice display severe immunodeficiencies, primarily of the T cell system (1, 2). It was unclear, however, whether there was a direct relationship between the deficiencies in growth hormone (GH) and prolactin (PRL) that these mice display and their immune system defects. Recently, Murphy et al. (3, 4) have demonstrated that DW/J mice, in addition to lacking acidophilic anterior pituitary cells, which results in virtually no GH or PRL production as well as thyroid stimulating hormone (TSH) and adrenocorticotrophic hormone (ACTH) deficiencies, have significant defects in thymic development. Specifically, the thymuses of DW/J mice lack CD4+CD8+ double-positive T cell precursors that differentiate into both CD4+ helper/inducer cells and CD8+ cytotoxic/ suppressor cells. Treatment of DW/J mice with GH partially restores the CD4+CD8+ precursors in the thymus, while PRL treatment decreases thymic size, but increases the number of peripheral blood T cells and enhances their proliferative responses following activation by both a mitogen and antigen. Thus, while both GH and PRL affect the immune system, they appear to influence different cell populations. Similar, but less detailed, findings have also been reported in GH-deficient Ames dwarf mice (5).