Following activation in vitro, peripheral blood mononuclear cells (PBMC) express cell-associated interleukin-2 receptors (IL-2R) and also release soluble IL-2R into culture supernatants. The present studies were undertaken to define which normal cells were responsible for the release of soluble IL-2R in vitro. Both cell-associated and soluble IL-2R were quantitatively measured with a "sandwich" enzyme-linked immunoassay employing two monoclonal antibodies. PBMC were separated into populations of surface immunoglobulin-negative cells (T cells and monocytes) and surface immunoglobulin-positive cells (B cells and monocytes), and the T-cell population was further separated into OKT4-positive (OKT4+) cells and OKT4-negative (OKT4-) cells. Following activation with phytohemagglutinin, pokeweed mitogen, and the monoclonal antibody OKT3, large amounts of soluble IL-2R were released by PBMC, unseparated T cells, OKT4+ T cells, and OKT4- T cells. The population containing B cells and monocytes made small but readily detectable amounts of soluble IL-2R when stimulated with these T-cell mitogens; likely the result of contaminating T cells in the population. However, when highly purified B cells were stimulated with Staphylococcus aureus Cowan and recombinant IL-2, they also released small amounts of soluble IL-2R. The release of soluble IL-2R by T cells appeared monocyte dependent when OKT3, but not phytohemagglutinin, was employed for activation, and monocytes themselves released no detectable IL-2R under the conditions employed. These studies define the cellular requirements for the release of soluble IL-2R in vitro and demonstrate that such receptors are released by B cells, T cells, and both OKT4+ and OKT4- T-cell subsets.

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We report our experience concerning clinical and paraclinical features of multiple sclerosis in 19 children. The disease was highly variable in its presentation but acute episodes of retrobulbar optic neuritis or transverse myelitis or cerebellitis were commonly observed at the onset. Diagnosis was very often suspected as soon as the first episode when there was clinical evidence of more than one lesion (43%) or study of the cerebrospinal fluid demonstrated a local secretion of immunoglobulins (60%). Evoked potential studies and nuclear magnetic resonance imaging were performed during the course of the disease and exhibited abnormalities of the kind observed in adult patients and with a similar frequency; this suggests that such studies can be very useful in the evaluation of children suspected of having multiple sclerosis. When the initial form of the disease was a chronic myelopathy, the course was progressive from the onset, leading rapidly to a marked invalidity (15%). Most often a succession of relapses and remissions occurred after the first attack and major sequelae appeared 5 to 10 years later. Such features are not very different from those observed in adult patients and suggest that these patients can benefit from the progress resulting from therapeutic trials in adult patients.

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