{'fraction_non_alphanumeric': 0.03670634920634921, 'fraction_numerical': 0.018849206349206348, 'mean_word_length': 4.668539325842697, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Prostaglandin E2 and IL-4 provide naive CD4+ T cells with distinct inhibitory signals for the priming of IFN-gamma production.

We investigated the effects of prostaglandin E2 and IL-4 on the acquisition of cytokine-producing ability by naive CD4(+) T cells in human umbilical cord blood. The presence of PGE2 or IL-4 at primary stimulation inhibited the production of IFN-gamma at secondary stimulation, and the combination of these stimuli resulted in cooperative effects. During primary stimulation with anti-CD3, the intracellular cAMP level was elevated in PGE2-treated cells but not in IL-4-treated or control cells. The signal provided by PGE2, but not by IL-4, was inhibited with RpcAMP, indicating that it was mediated by cAMP. After differentiation into Th2-like cells, cAMP levels in PGE2- and IL-4-treated cells were not different. Our results suggest that both PGE2 and IL-4 play important roles with distinct mechanisms in inhibiting the priming of IFN-gamma production of naive CD4(+) T cells.