Growth hormone restores glucocorticoid‐induced T cell suppression

Dobashi, Hiroaki; Sato, Makoto; Tanaka, Terukazu; Tokuda, Michiaki; Ishida, Toshihiko

doi:10.1096/fj.00-0702fje

Cited by 28 publications

(14 citation statements)

References 41 publications

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“…Interestingly, we previously reported that hGH prevented glucocorticoid-induced apoptosis in human peripheral T lymphocytes. This antiapoptotic effect, however, was detected in CD4+ but not in CD8+ T lymphocytes [24]. hGH enhanced the expression of Bcl-2 at both the protein and mRNA level in human peripheral CD4+ T lymphocytes.…”

Section: Discussionmentioning

confidence: 77%

Growth Hormone Prevents Fas-Induced Apoptosis in Lymphocytes through Modulation of Bcl-2 and Caspase-3

Mitsunaka¹,

Dobashi²,

Sato³

et al. 2001

Neuroimmunomodulation

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Objective: Growth hormone (GH) has been reported to have a potent effect on the immune system. However, the detailed mechanism of the effect of GH on the immune system has not yet been clarified. This study was designed to investigate the nature of this mechanism. Methods: In the present study, we investigated the effects of GH on the susceptibility of both human CEM/C7 lymphocytes and human IM-9 lymphocytes to Fas-induced apoptosis. Results: Both cell lines expressed GH receptor mRNA. GH rescued Fas-induced suppression of [³H]-thymidine incorporation into each cell line. GH prevented Fas-induced apoptosis in each cell line without changing Fas antigen expression. We next investigated the mechanisms of the prevention of Fas-induced apoptosis, by focusing on intracellular molecules related to the apoptotic signal. Bcl-2 expression was increased by GH treatment in both CEM/C7 and IM-9 lymphocytes. GH also downregulated caspase-3 expression and inhibited activation of caspase-3 in both cell lines. Conclusion: These findings suggest that GH regulates the human immune system through inhibition of Fas-induced apoptosis in activated T and B lymphocytes.

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Section: Discussionmentioning

confidence: 77%

Growth Hormone Prevents Fas-Induced Apoptosis in Lymphocytes through Modulation of Bcl-2 and Caspase-3

Mitsunaka¹,

Dobashi²,

Sato³

et al. 2001

Neuroimmunomodulation

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“…LEC treatment with GH inhibited LEC apoptosis, in accordance with previous results in other cell types including mammary carcinoma cells 49 and in T cells. 50 Previous studies have indicated that several lymphangiogenic factors might mediate their effects on LECs indirectly via paracrine or autocrine effects leading to activation of VEGFR-2 or VEGFR-3. In particular, the lymphangiogenic activity of basic fibroblast growth factor was inhibited by blockade of VEGFR-3 signaling.…”

Section: Discussionmentioning

confidence: 99%

Growth Hormone Promotes Lymphangiogenesis

Bänziger-Tobler

Halin

Kajiya

et al. 2008

The American Journal of Pathology

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The lymphatic system plays an important role in inflammation and cancer progression, although the molecular mechanisms involved are poorly understood. As determined using comparative transcriptional profiling studies of cultured lymphatic endothelial cells versus blood vascular endothelial cells, growth hormone receptor was expressed at much higher levels in lymphatic endothelial cells than in blood vascular endothelial cells. These findings were confirmed by quantitative real-time reverse transcriptase-polymerase chain reaction and Western blot analyses. Growth hormone induced in vitro proliferation, sprouting, tube formation, and migration of lymphatic endothelial cells, and the mitogenic effect was independent of vascular endothelial growth factor receptor-2 or -3 activation. Growth hormone also inhibited serum starvation-induced lymphatic endothelial cell apoptosis. No major alterations of lymphatic vessels were detected in the normal skin of bovine growth hormone-transgenic mice. However, transgenic delivery of growth hormone accelerated lymphatic vessel ingrowth into the granulation tissue of full-thickness skin wounds, and intradermal delivery of growth hormone resulted in enlargement and enhanced proliferation of cutaneous lymphatic vessels in wild-type mice. These results identify growth hormone as a novel lymphangiogenic factor. (Am J

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“…A common clinical result of this change in the hormonecytokine ratio is that the biological effect of the hormone is impaired by a proinflammatory cytokine, thereby leading to endocrine resistance. For example, dexamethasone inhibits proliferation of human T cells, and this effect is partially reversed by increasing the ratio of hormones by addition of exogenous GH and IGF-I (Dobashi et al, 2001). Unfortunately, we do not yet know the critical events that occur inside proliferating T cells when they are exposed to both IGF-I and dexamethasone.…”

Section: And Beyondmentioning

confidence: 99%

Protein hormones and immunity

Kelley

Weigent

Kooijman³

2007

Brain, Behavior, and Immunity

191

117

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A number of observations and discoveries over the past 20 years support the concept of important physiological interactions between the endocrine and immune systems. The best known pathway for transmission of information from the immune system to the neuroendocrine system is humoral in the form of cytokines, although neural transmission via the afferent vagus is well documented also. In the other direction, efferent signals from the nervous system to the immune system are conveyed by both the neuroendocrine and autonomic nervous systems. Communication is possible because the nervous and immune systems share a common biochemical language involving shared ligands and receptors, including neurotransmitters, neuropeptides, growth factors, neuroendocrine hormones and cytokines. This means that the brain functions as an immune-regulating organ participating in immune responses. A great deal of evidence has accumulated and confirmed that hormones secreted by the neuroendocrine system play an important role in communication and regulation of the cells of the immune system. Among protein hormones, this has been most clearly documented for prolactin (PRL), growth hormone (GH), and insulin-like growth factor-1 (IGF-I), but significant influences on immunity by thyroid stimulating hormone (TSH) have also been demonstrated. Here we review evidence obtained during the past 20 years to clearly demonstrate that neuroendocrine protein hormones influence immunity and that immune processes affect the neuroendocrine system. New findings highlight a previously undiscovered route of communication between the immune and endocrine systems that is now known to occur at the cellular level. This communication system is activated when inflammatory processes induced by proinflammatory cytokines antagonize the function of a variety of hormones, which then causes endocrine resistance in both the periphery and brain. Homeostasis during inflammation is achieved by a balance between cytokines and endocrine hormones.

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Growth hormone restores glucocorticoid‐induced T cell suppression

Cited by 28 publications

References 41 publications

Growth Hormone Prevents Fas-Induced Apoptosis in Lymphocytes through Modulation of Bcl-2 and Caspase-3

Growth Hormone Prevents Fas-Induced Apoptosis in Lymphocytes through Modulation of Bcl-2 and Caspase-3

Growth Hormone Promotes Lymphangiogenesis

Protein hormones and immunity

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