The thymus is the principal organ of T cell production and Growth hormone (GH) is a potent regulator of thymic function.
Evidence suggests a two-way correlation between the neuroendocrine system and the immune system. It is well known that lymphoid organs such as the thymus, the spleen, and peripheral blood generate growth hormone. GH receptors are found on distinct groups of lymphocytes.
GH encourages the proliferation of T and B cells and the synthesis of immunoglobulin. It also accelerates the evolution of myeloid progenitor cells while also modulating cytokine response.
Numerous pieces of evidence from Research has reported the bi-directional relationship between the Growth Hormone and the Immune System. In both in vivo and in vitro studies in animal and human studies, interactions have been evidenced between growth hormone and the immune system.
With age, the thymus gland begins to atrophy. Aging-related thymus atrophy results in an increased incidence of autoimmune and infectious conditions in the human body.
Parallel to the thymus gland shrinkage, a decline in the number of T-cells and immune factors like Interleukin 2 occurs.
As researchers debated the role of growth hormone in immunity and thymic function, a study was conducted to determine whether the thymic function can be induced in HIV infected adults by Growth Hormones. The study also aimed to confirm that such induction is actually driven by growth hormone. Additionally, the study planned to evaluate whether thymic function plays a role in sustaining the T cell compartment.
Participants: Twenty-four volunteers were enrolled in the 2-year study.
Methodology: All participants received 12 months of treatment with human growth hormone. Participants were randomly assigned to one of two study groups. Twelve participants (Group 1) received growth hormone during the first year of the study. Twelve participants (Group 2) were enrolled in an observational control group that crossed over to growth hormone treatment after 1 year. Each Study visit included physical exams, blood tests, CT scans, PET scans, and DEXA scans.
Conclusion: GH treatment was associated with increased circulating levels of IGF-1.
GH treatment resulted in significant radiographic changes in the thymus gland by therapy duration of 6 months, as well as sizeable increases in circulating naive T cells, signifying improved thymic function.
GH treatment is associated with an increase in thymopoiesis and recovery in peripheral T cells. Many of the immune effects seem to be mediated by IGF-1, therefore it is possible that GH or IGF-1 also stimulates gains in T cell number by enhancing the expansion of peripheral T cell synthesis.
In the immunodeficient and aging population, HGH therapy may play a particularly important role in improving thymus gland function and as a result the ability of the immune system to fight viral, bacterial, and fungal infections.