Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THYMUS GLAND”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources
PubMedDate not supplied

[Acetylcholinesterase activity and catecholamine content in nerve fibers of the thymus gland and spleen in white rats at remote time after chronic exposure to physical factors and administration of interleukin-1 beta].

Acetylcholinesterase (AChE) activity and catecholamine (CA) content in nerve fibres of the thymus and spleen of white rats were studied 6 months after prolonged combined exposure to ionizing radiation and heat and after application of interleukin-1 beta (IL-1 beta). Combined action of the physical factors induced a certain decrease in AChE activity and increase in CA content in both organs. Application of the cytokine to animals exposed to radiation and heat elicited a more pronounced decrease in AChE in these lymphoid organs and increase, especially in the spleen, in CA. The results suggest about enhanced responsiveness of the autonomic nervous system to IL-1 beta animals which had been long before exposed to prolonged combined action of radiation and heat.

Acetylcholinesterase↗
PubMed2002

The thymus gland: a target organ for growth hormone.

Increasing evidence has placed hormones and neuropeptides among potent immunomodulators, in both health and disease. Herein, we focus on the effects of growth hormone (GH) upon the thymus. Exogenous GH enhances thymic microenvironmental cell-derived secretory products such as cytokines and thymic hormones. Moreover, GH increases thymic epithelial cell (TEC) proliferation in vitro, and exhibits a synergistic effect with anti-CD3 in stimulating thymocyte proliferation, which is in keeping with the data showing that transgenic mice overexpressing GH or GH-releasing hormone exhibit overgrowth of the thymus. GH also influences thymocyte traffic: it increases human T-cell progenitor engraftment into the thymus; augments TEC/thymocyte adhesion and the traffic of thymocytes in the lymphoepithelial complexes, the thymic nurse cells; modulates in vivo the homing of recent thymic emigrants, enhancing the numbers of fluroscein isothiocyanate (FITC)+ cells in the lymph nodes and diminishing them in the spleen. In keeping with the effects of GH upon thymic cells is the detection of GH receptors in both TEC and thymocytes. Additionally, data indicate that insulin-like growth factor (IGF)-1 is involved in several effects of GH in the thymus, including the modulation of thymulin secretion, TEC proliferation as well as thymocyte/TEC adhesion. This is in keeping with the demonstration of IGF-1 production and expression of IGF-1 by TEC and thymocytes. Also, it should be envisioned as an intrathymic circuitry, involving not only IGF-1, but also GH itself, as intrathymic GH expression is seen both in TEC and in thymocytes, and that thymocyte-derived GH could enhance thymocyte proliferation. Finally, the possibility that GH improve thymic functions, including thymocyte proliferation and migration, places this molecule as a potential therapeutic adjuvant in immunodeficiency conditions associated with thymocyte decrease and loss of peripheral T cells.

Animals↗