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This report describes two types of reticular epithelial cell in the thymic cortex of the BALB/c mouse, an immature and a mature form. During early stages of lymphoma development, i.e., 2-6 weeks postinfection (p.i.) with Moloney leukemia virus (M-MuLV), activation of the epithelial cells is observed. Although the percentage of these cells in the total cell population of the thymic cortex remains constant during that time, the number of mature epithelial cells is significantly increased in infected animals. Subsequently, about 6 weeks p.i., the number of immature epithelial cells starts to increase, whereas the number of mature reticular epithelial cells declines and the appearance of the mature epithelial cells changes drastically. The results of light and electron microscopic studies indicate degeneration of the mature reticular epithelial cells at the onset of lymphoma development at a time when the first deficiencies in the immunologic competence of the reticular epithelial cells are apparent. [ABSTRACT FROM AUTHOR]

Previous cytokinetic studies in Moloney-virus (M-MuLV)-induced lymphomas of BALB/c mice showed an intrathymic maturation block of prethymic lymphocytes derived from hematopoietic tissues. Thymus-cell cultures during the latent period of lymphoma development showed a proportion of nonlymphoid cells (NLC) from uninfected mice of 0.1% (3 days) to 0.002% (20 days), rising in infected mice to 1-2% after 5 weeks. Concomitantly, thymic epithelial cells exhibit progressive degenerative changes in vivo in infected mice with virus replication and in vitro a marked cellular polymorphism with nuclear atypia becomes overt. Immunofluorescence studies of thymopoietin II and serum thymus factor in epithelial cells indicate a marked decrease of these hormones in the epithelial cells from infected mice. These results suggest a functional defect of virus-infected thymic epithelial cells which causes a progressive accumulation of nondifferentiating T-cell precursors. [ABSTRACT FROM AUTHOR]

The regulatory role of retinoids in growth and differentiation has been examined in vitro and in vivo by light and scanning electron microscopy using retinoid-deficient and control quail embryos between the 5-15 somite stage, as well as 2- and 2.5-day-old embryos. Fertile, retinoid-deficient eggs were obtained from flocks of quail maintained on a retinoid- and carotenoid-deficient diet, supplemented only with small amounts of retinoic acid methyl ester as described by Thompson et al. 1969. As described previously, retinoid deprivation during embryonal development causes abnormalities in organs of epithelial and mesenchymal origin, most dramatically preventing the formation of the extraembryonal circulatory system in the avian embryo. Our in vivo studies show that the basis for the latter defect is the failure of the primitive heart tubes to open at their posterior end, thus preventing the formation of omphalomesenteric veins normally connecting the embryonal with the extraembryonal circulatory system. Early manifestation of the retinoid-deficient defect may result also in formation of a cardia bifida, late manifestation in development of a single dilated ventricle. In contrast, the extraembryonal vascular system of blood islands is well developed. Heart function as shown by the rate of heart beat is reduced in deficient embryos. Our in vitro studies demonstrate similar defects in the development of the circulatory system by culture of normal 24-h embryos on retinoid-deficient agar medium; conversely, normal development is observed upon culture of retinoid-deficient embryos on retinoid-containing agar medium. [ABSTRACT FROM AUTHOR]

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Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)