Abstract
THOMA WHARTON reported in 1656 in his book entitled Adenographia sive Glandularum Totius Corporis Descriptio that in young oxen put to work, the thymus becomes smaller than in controls at rest. At the beginning of our century, numerous studies related thymic atrophy in malnutrition and illness with cachexia (JOLLY and LEVIN 1911; JACKSON 1925; BOYD 1927, 1932). The reduction in the thymus size following a great variety of stimuli appeared to be secondary to a drastic pyknosis of thymocytes described by DUSTIN (1925) as “choc caryoclastique” (Karyoklastic shock). HAMMAR (1929) found that the thymus weight of children dying accidentally was considerably greater than in those dying of disease. BOYD (1932), in his extensive report on thymus in health and disease, pointed out that the thymus atrophy resulted from the disease. SELYE (1936) and, a little later, LEBLOND and SEGAL (1938) demonstrated the causal role played by the adrenals in the histological modifications of the thymus during “stress.” Functional and morphological alterations in lymphoid tissue induced by adrenocorticotropic hormone (ACTH) and mediated by the adrenal cortex were also well documented experimentally by DOUGHERTY and WHITE (1945).
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Dourov, N. (1986). Thymic Atrophy and Immune Deficiency in Malnutrition. In: Müller-Hermelink, H.K. (eds) The Human Thymus. Current Topics in Pathology, vol 75. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-82480-7_4
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