Growth Hormone Stimulates the Selective Trafficking of Thymic CD4+CD8– Emigrants to Peripheral Lymphoid Organs

Smaniotto, Salete; Ribeiro-Carvalho, Marilza Moura; Dardenne, Mireille; Savino, Wilson; Coelho, Valéria de Mello

doi:10.1159/000079410

Cited by 33 publications

(31 citation statements)

References 39 publications

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“…Although the preference for lymph nodes was observed for CD4 + RTE and CD8 + RTE cells, the CD4 + RTE subset seemed to be more affected. These results are in line with our previous work, where we utilized another immunostimulator agent, the growth hormone (GH) [35]. Thus, from a conceptual point of view, hormonal control of T-cell homing might be a complex process, probably involving different endocrine pathways.…”

Section: Discussionsupporting

confidence: 90%

“…+ RTE and CD8 + RTE in murine peripheral lymph nodes [35]. In this study, intrathymic T 3 treatment promoted only a tendency towards the increased expression of CD62L on CD4 + RTE and CD8 + RTE in peripheral lymph nodes, but not a significant difference.…”

Section: Cd4contrasting

confidence: 68%

“…Previously, we have shown that growth hormone stimulates T-cell homing to peripheral lymph nodes and upregulates CD62L on RTE [35]. In this study, we found that, without any stimulus or with T 3 treatment, the majority of RTE in lymph nodes seems to express this adhesion molecule.…”

Section: Influence Of T 3 On Cd62l Expression On Rte In Peripheral Lysupporting

confidence: 58%

“…By contrast, a significant decrease in the percentage of CD62L + CD4 + RTE was observed in the spleen of T 3 -treated mice in relation to control. As CD62L is not crucial for T-cell entrance in the spleen [35,40], this particular effect of T 3 may not be related to the migration of CD4 + RTE to this organ. Thus, our data suggest that CD62L does not seem to be involved in the T 3 -dependent preferential migration of RTE to the lymph nodes, which indicates that T 3 and GH might stimulate T-cell homing through distinct molecular mechanisms.…”

Section: Cd4mentioning

confidence: 99%

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Triiodothyronine Modulates Differential Homing of Recent Thymic Emigrants to Peripheral Lymphoid Organs

et al. 2007

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The functioning of the immune system partially relies on T‐cell exportation from the thymus, the major site of T‐cell differentiation. Although the molecular mechanisms governing this process begin to be elucidated, it is not clear if thyroid hormones can alter the homing of recent thymic emigrants (RTE) to peripheral lymphoid organs. Herein, we investigated whether triiodothyronine (T3) could influence the homing of thymus‐derived T cells. For that we used intrathymic injection of T3 in combination with fluorescein isothiocyanate (FITC) to trace, 16 h later, FITC+ cells, termed RTE, in peripheral lymphoid organs. We observed that T3 stimulated thymocyte export, increasing the frequency of CD4+ RTE and CD8+ RTE in the subcutaneous and mesenteric lymph nodes. By contrast, the relative numbers of CD4+ RTE in the spleen were decreased. T3 also changed the differential distribution pattern of CD4+ RTE, and to a lesser extent CD8+ RTE in the peripheral lymphoid organs. Moreover, the expression of extracellular matrix (ECM) components, such as laminin and fibronectin, which are known to be involved in T‐cell migration, increased in the lymph nodes but not in the spleen following intrathymic T3 treatment. In conclusion, our data correspond to the first demonstration that in vivo treatment with thyroid hormone stimulates thymic T‐cell homing and T‐cell distribution in peripheral lymphoid organs.

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Section: Discussionsupporting

confidence: 90%

Section: Cd4contrasting

confidence: 68%

Section: Influence Of T 3 On Cd62l Expression On Rte In Peripheral Lysupporting

confidence: 58%

Section: Cd4mentioning

confidence: 99%

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Triiodothyronine Modulates Differential Homing of Recent Thymic Emigrants to Peripheral Lymphoid Organs

et al. 2007

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“…Another possible explanation for the unexpectedly low frequency of naive T cell TRECs is that GH treatment led to altered trafficking of RTEs. Thus, murine studies have demonstrated that GH therapy promotes the accumulation of RTEs in peripheral lymphoid tissues by increasing RTE expression of adhesion molecules (49,50). IL-7 and thyroid hormone also have been found to promote accumulation of TREC-bearing naive T cells and RTEs in lymphoid tissues (51,52).…”

Section: Discussionmentioning

confidence: 99%

Growth hormone enhances thymic function in HIV-1–infected adults

et al. 2008

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Growth hormone (GH) is an underappreciated but important regulator of T cell development that can reverse age-related declines in thymopoiesis in rodents. Here, we report findings of a prospective randomized study examining the effects of GH on the immune system of HIV-1-infected adults. GH treatment was associated with increased thymic mass. In addition, GH treatment enhanced thymic output, as measured by both the frequency of T cell receptor rearrangement excision circles in circulating T cells and the numbers of circulating naive and total CD4 + T cells. These findings provide compelling evidence that GH induces de novo T cell production and may, accordingly, facilitate CD4 + T cell recovery in HIV-1-infected adults. Further, these randomized, prospective data have shown that thymic involution can be pharmacologically reversed in humans, suggesting that immune-based therapies could be used to enhance thymopoiesis in immunodeficient individuals.

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Resident murine macrophage migration and phagocytosis are modulated by growth hormone

Reis

Santos

Menezes

et al. 2018

Cell Biology International

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Growth hormone (GH) plays a physiological role in the immune system. In macrophages, GH enhances the production of hydrogen peroxide, superoxide anions, nitric oxide, cytokines, and chemokines, including interferon-γ and macrophage inflammatory protein-1α. However, some of the effects of GH stimulation on the biological functions of macrophages remain to be elucidated. Herein, we showed that in vivo GH treatment resulted in decreased expression of VLA-5 and VLA-6 integrins on the macrophage surface, accompanied by a reduction in macrophage adhesion to extracellular matrix (ECM) ligands, fibronectin, and laminin. Additionally, a decrease in macrophage adhesion to laminin was observed when the cells were treated in vitro with GH. In transwell migration assays, GH-treated macrophages showed increased migration after 6 h. Although in vitro GH treatment did not influence the phagocytic activity of macrophages, when the treatment was performed in vivo, peritoneal macrophages from GH-treated mice showed a higher percentage of phagocytosis and higher phagocytic capacity than cells from control animals. These results led us to analyse the role of insulin-like growth factor-1 (IGF-1), a GH stimulated factor, on macrophage phagocytosis. We observed an increase in phagocytic activity when J774 murine macrophages were treated with IGF-1 for 24 h. Our results revealed an important role for GH in resident macrophage migration and phagocytic activity. Specifically, we demonstrate that IGF-1 may be the GH stimulated factor that induces macrophage phagocytosis in vivo.

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Growth Hormone Stimulates the Selective Trafficking of Thymic CD4+CD8– Emigrants to Peripheral Lymphoid Organs

Cited by 33 publications

References 39 publications

Triiodothyronine Modulates Differential Homing of Recent Thymic Emigrants to Peripheral Lymphoid Organs

Triiodothyronine Modulates Differential Homing of Recent Thymic Emigrants to Peripheral Lymphoid Organs

Growth hormone enhances thymic function in HIV-1–infected adults

Resident murine macrophage migration and phagocytosis are modulated by growth hormone

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