Requirements for activation of human peripheral blood T cells by mouse monoclonal antibodies to CD3.

The present study was undertaken in an attempt to reconcile the conflicting results concerning the signals required for the activation of human resting T cells by antibodies to the T-cell receptor/CD3 complex (Ti/CD3). For this purpose we have used highly purified peripheral blood T cells, depleted of monocytes and of preactivated Ia + T cells, to the extent that they were unable to proliferate to interleukin 2 (IL-2) alone or to optimal doses of phytohemagglutinin (PHA). To further minimize the contribution of contaminating monocytes, we used the anti-CD3 mAb, Leu-4, and cells from Leu-4 nonresponder subjects, whose monocytes we show completely fail to bind the Leu-4 mAb.

Antigen presentation by human dermal fibroblasts: activation of resting T lymphocytes.

We have shown that human dermal fibroblasts, exposed to interferon-gamma (IFN-gamma) to induce surface class II major histocompatibility complex (MHC) antigens, were capable of presenting tetanus toxoid (TT) antigen to human TT-specific T cell clones. Antigen presentation by fibroblasts was antigen dependent, required HLA-DR expression by fibroblasts, and was MHC restricted. In contrast, we now report that IFN-gamma-treated fibroblasts are unable to present TT antigen to purified resting T cells obtained from the peripheral blood of TT-immune donors.

Hypereosinophilia and recurrent angioneurotic edema in a 2 1/2-year-old girl.

A 2 1/2-year-old girl presented with monthly episodes of angioneurotic edema, eruption of pruritic papules, and fever. During acute episodes, white blood cell counts rose as high as 52,100/cu mm with 62% eosinophils, and body weights increased up to 20% of remission weight. Short courses of prednisone acetate caused rapid defervescence, resolution of angioneurotic edema, and lowering of eosinophil counts.

Mechanisms of human T cell response to mitogens: IL 2 induces IL 2 receptor expression and proliferation but not IL 2 synthesis in PHA-stimulated T cells.

Human peripheral blood T cells were purified by a four-step procedure which included depletion of plastic-adherent cells, rosetting with sheep red blood cells, nylon wool passage, and treatment with mouse monoclonal antibodies to human Ia antigens plus complement. The purified T cells completely failed to proliferate to phytohemagglutinin (PHA). Bacterially derived recombinant human interleukin 2 (IL 2) reconstituted the proliferative response of resting T cells to PHA.

Distribution of prostaglandin E 9-ketoreductase and NAD+-dependent and NADP+-dependent 15-hydroxyprostaglandin dehydrogenase in the renal cortex and medulla of various species.

Regional distributions of PGE 9-ketoreductase and 15-hydroxy-prostaglandin dehydrogenase were examined in the cytoplasmic fractions from the kidneys of seven species. All species contained an NADPH-dependent reductase, as well as NAD+- and NADP+-dependent dehydrogenases in both cortex and medulla. A previously unrecognized cytoplasmic NADH-dependent PGE 9-ketoreductase was also detected in the cortex and medulla of rat and bovine kidney.

Distribution of prostaglandin E 9-KETOREDUCTASE AND TYPES I and II 15-hydroxyprostaglandin dehydrogenase in swine kidney medulla and cortex.

Prostaglandin E 9-ketoreductase, NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (type I), and NADP+-dependent 15-hydroxyprostaglandin dehydrogenase (type II) have been partially purified from swine renal medulla and cortex. Eleven times more NAD+-dependent 15-hydroxyprostaglandin dehydrogenase activity was found in the cortex than in the medulla. On the other hand, about twice as much NADP+-dependent dehydrogenase activity was found in the medulla than in the cortex.