Evidence for the involvement of corticosterone in the ontogeny of the cellular immune apparatus of the mouse.
The effects of corticosterone deprivation in the cellular immune system of the mouse have been studied. Adrenalectomy was performed from three weeks after birth; at an earlier age oral administration of aminoglutethimide phosphate (AGP) had to be used. Three effects could be recognized: (1) Adrenalectomy or AGP treatment, at any age studied, resulted in an enhanced delayed hypersensitivity (DH) to sheep red blood cells (SRBC). This effect has previously been ascribed to monocytes. (2) An altered T lymphocyte distribution was observed as consequence of early adrenalectomy or continuous AGP administration. The lymph nodes were depleted whereas the thymus was increased in size and blood-leucocytes increased in number. This effect appeared reversible on restoration of adrenal function. (3) Irreversible damage to the cellular immune system following early AGP intake was observed in DH after recovery of the adrenal function. As corticosterone is the principal glucocorticoid produced by mice the effects described under (2) and (3) may be ascribed to this hormone. Our results suggest that thymic involution during life, is at least partially, under adrenal control.
D000311:Adrenal Glands / Q000033:anatomy & histology; D000315:Adrenalectomy; D000616:Aminoglutethimide / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000502:physiology*; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007111:Immunity, Cellular / Q000187:drug effects; D007958:Leukocyte Count; D008221:Lymphoid Tissue / Q000033:anatomy & histology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009929:Organ Size / Q000187:drug effects; D013601:T-Lymphocytes / Q000276:immunology
D000616:Aminoglutethimide; D003345:Corticosterone