Relationship between Developmental Hormones, the Thymus, and Immunological Capacity

Abstract

Recent findings have shown that thymus atrophy can be induced in young mice by a single intraperitoneal injection of rabbit antimouse pituitary serum. These mice also show inhibition of body growth and a cachectic syndrome with features similar to those in mice wasting after neonatal thymectomy [1]. It was observed that the degree of thymus involution with concomitant loss of small lymphocytes in the cortex parallels the inhibition of body growth. In animals which overcome the syndrome and gain weight, a repopulation of the thymus cortex and normalization of the thymus structure and weight is observed [2]. It has been shown that this antipituitary serum contains antibodies directed against the acidophilic, growth hormone-producing cells of the mouse anterior pituitary [3]. The observation of a degranulation of acidophils in the pituitary gland of neonatally thymectomized mice [4] and the findings on the reconstitution produced by gonadectomy in lymphoid tissue of neonatally thymectomized mice [5] have suggested that perinatal thymus is under direct or indirect influence of one or several hypophyseal hormones. These hormones are probably responsible for the turnover of the cells of the thymus cortex and for the high mitotic rate of this organ in the period of body growth until and after sexual maturation [2, 4]. The concept of perinatal thymus as target gland of the hypophysis has been strengthened by the observation that hereditary pituitary dwarf mice have a hypotrophic thymus and peripheral lymphoid tissue [6, 7].