期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 107, 期 2, 页码 821-826出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0909235107
关键词
IL-4 signal; immunoglobulin; germ-line transcription
资金
- National Institutes of Health [R01 AI54821]
- Arthritis Foundation
IL-4 signaling promotes IgE class switching through STAT6 activation and the induction of Ig germ-line epsilon (GL epsilon) transcription. Previously, we and others identified a transcription factor, Nfil3, as a gene induced by IL-4 stimulation in B cells. However, the precise roles of nuclear factor, IL-3-regulated (NFIL3) in IL-4 signaling are unknown. Here, we report that NFIL3 is important for IgE class switching. NFIL3-deficient mice show impaired IgE class switching, and this defect is B-cell intrinsic. The induction of GL epsilon transcripts after LPS and IL-4 stimulation is significantly reduced in NFIL3-deficient B cells. Expression of NFIL3 in NFIL3-deficient B cells restores the impairment of IgE production, and overexpression of NFIL3 in the presence of cycloheximide induces GL epsilon transcripts. Moreover, NFIL3 binds to I epsilon promoter in vivo. Together, these results identify NFIL3 as a key regulator of IL-4-induced GL epsilon transcription in response to IL-4 and subsequent IgE class switching.
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