Treatment of erythrocytes with the thiolspecific oxidant azodicarboxylic acid bis(dimethylamide) (diamide) enhances their phagocytosis by adherent monocytes. Phagocytosis of diamide-treated erythrocytes required that the cells were opsonized with whole serum, since complement inactivation abolished phagocytosis. Opsonization with whole serum containing 20-100 times the physiological concentration of naturally occurring anti-band-3 antibodies enhanced phagocytosis of diamide-treated erythrocytes. High inputs of antiband-3 also restored phagocytosis oferythrocytes that had been incubated with complement-inactivated serum. Elevated concentrations of anti-spectrin antibodies were ineffective in whole and complement-inactivated serum.
IL-12 is a cytokine produced by monocytes and Epstein-Barr virus-transformed B cells which initiates Th1 responses by inducing the development of CD4+, IFN-gamma producing Th1 T cells in mouse and human. We have previously reported that allergen-specific CD4+ Th2 T cell clones produce IFN-gamma, following activation by phorbol ester (TPA) and calcium ionophore, indicating that these cells still have the ability to produce IFN-gamma. This observation, together with the capacity of IL-12 to induce IFN-gamma, prompted us to examine the effects of rIL-12 on the cytokine production profiles of a panel of cloned allergen-specific Th2 cell lines, and compare these to the effects of rIL-12 on the cytokine production by Th0 and Th1 T cell clones. Activation with antigen or TPA/anti-CD3 mAb of Th2 T cell clones that had been preincubated with rIL-12 and rIL-2 for 5 days induced or enhanced the expression of IFN-gamma transcripts, as well as the production of IFN-gamma by these cells. Furthermore, in a different set of experiments, it was found that the presence of rIL-12 during a 12 h stimulation of Th2 T cell clones induced or enhanced the expression of IFN-gamma transcripts, as well as the production of IFN-gamma by these cells. rIL-12 also enhanced IFN-gamma production by Th0 and Th1 T cells, but, in contrast, rIL-12 had no effect on the production of IL-4, nor on the frequency of IL-4 producing cells, as judged by analysis of intracellularly produced cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)
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