{'fraction_non_alphanumeric': 0.0328381548084441, 'fraction_numerical': 0.012509773260359656, 'mean_word_length': 4.638766519823789, '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}}
Induction of the IL-7 receptor alpha chain in mouse peripheral B cells by glucocorticoids.

Expression of the IL-7R alpha chain (IL-7R alpha) is strictly regulated during development and maturation of lymphocytes. While T cells express the IL-7R alpha in the periphery, B cells do not. Glucocorticoids (GCs) have pleiotypic effects on development and function of lymphocytes. Although GCs induce the transcription of IL-7R alpha gene in T cells, their effect on B cells is largely unknown. Here, we show that GCs induce the transcription and expression of IL-7R alpha in mouse peripheral B cells. This effect does not require de novo protein synthesis, because a protein synthesis inhibitor, cycloheximide, does not block the transcription. IL-7R signal pathway is intact in peripheral B cells because Stat5, one of the signal molecules of the IL-7R alpha, is phosphorylated by IL-7 stimulation. We also observed that IL-7 simulation induces the transcription of Cis-1, one of the target genes of Stat5. Furthermore, GC-induced IL-7R alpha can transmit survival signal in B cells. Therefore, this study demonstrates that GCs induce the transcription and expression of functional IL-7R alpha in peripheral B cells, and implies a potential role of the IL-7R in survival of B cells.