No abstract

Some activities of retinoids on cellular and humoral immunity have been described, but the available data are conflicting or obtained at concentrations that are toxic in vivo. In this study, we demonstrate that 13-cis-retinoic acid (13-cRA), a retinoid well tolerated in human therapy, can suppress T cell-mediated immunity in rats. Treatment with pharmacological concentrations of 13-cRA prevented active as well as passive transfer experimental autoimmune encephalomyelitis (EAE) and suppressed lymphocyte responsiveness to T cell mitogens, suggesting that the drug activity included suppression of an effector T cell response. In addition, mitogen-and antigen-induced lymphocyte proliferation was inhibited in vitro in the presence of concentrations of 13-cRA equivalent to or less than those achieved in vivo, further suggesting that the prevention of EAE was due to a suppressive activity on T cell-mediated immunity. The immunosuppressive activity of 13-cRA included suppression of interleukin 2, whose production was inhibited in splenocytes. These data indicate that, in an in vivo mammalian system, 13-cRA exerts a suppressive activity on T cell-mediated immunity intensive enough to suppress an ongoing immune response, and that this effect can be achieved at nontoxic concentrations that may also be attained in human therapy. (J. Clin.

Different degrees of cerebral calcifications together with encephalofacial angiomatosis and seizure disorder characterize the Sturge-Weber syndrome. According to the observations reported in the literature, calcium deposits may be found in the wall of cerebral vessels, in the perivascular tissue and rarely within the neurons. Corresponding to the variety of localizations, the interpretation of the phenomenon remains obscure. Most theories postulate the role of a vascular factor and of a mesenchymal factor. Ultramicroscopic studies of the specimens obtained in 2 children with the Sturge-Weber syndrome provided the following findings. A mucopolysaccharidic substance constitutes the substratum for the deposition of calcium. Small amounts of this substance and calcium deposits may be detected within the connective tissue of cerebral vessels precociously; later on, while increasing in size and calcium concentration, they obviously migrate to outside the vessels. Successively, the calcium deposits seem to localize around the blood vessels. In our opinion, these observations stress the role of a primitive vascular factor; consequently, anoxia, necrosis of cerebral tissues, and variation in the calcium ion concentration would act only as secondary factors.

No abstract

A neuropathological study was carried out in 4 cases of ischemic stroke with leuko-araiosis (LA), 3 cases of clinically suspected Binswanger’s subcortical arteriosclerotic encephalopathy (SAE) also showing LA, and 3 cases without LA. Unlike the SAE cases, in 3 of the cases in the first group the white matter changes corresponding to LA could not be explained by ischemic mechanisms related to small vessel changes.