IFN‐γ‐mediated inhibition of antigen receptor‐induced B cell proliferation and CREB‐1 binding activity requires STAT‐1 transcription factor
F Frissora, HC Chen, J Durbin… - European journal of …, 2003 - Wiley Online Library
F Frissora, HC Chen, J Durbin, S Bondada, N Muthusamy
European journal of immunology, 2003•Wiley Online LibraryWe report here a role for cyclic AMP‐responsive element‐binding protein‐1 (CREB‐1) in B
cell antigen receptor (BCR)‐induced growth inhibition by IFN‐γ. BCR‐induced proliferation
is negatively regulated by IFN‐γ. Stimulation through BCR resulted in dose‐dependent
induction of CREB‐1 binding to the consensus cyclic AMP‐responsive element.
Recombinant IFN‐γ inhibited the BCR‐induced CREB‐1 DNA binding activity and cell
proliferation in B cells from signal transducer and activator of transcription‐1 (STAT‐1)+/+ …
cell antigen receptor (BCR)‐induced growth inhibition by IFN‐γ. BCR‐induced proliferation
is negatively regulated by IFN‐γ. Stimulation through BCR resulted in dose‐dependent
induction of CREB‐1 binding to the consensus cyclic AMP‐responsive element.
Recombinant IFN‐γ inhibited the BCR‐induced CREB‐1 DNA binding activity and cell
proliferation in B cells from signal transducer and activator of transcription‐1 (STAT‐1)+/+ …
Abstract
We report here a role for cyclic AMP‐responsive element‐binding protein‐1 (CREB‐1) in B cell antigen receptor (BCR)‐induced growth inhibition by IFN‐γ. BCR‐induced proliferation is negatively regulated by IFN‐γ. Stimulation through BCR resulted in dose‐dependent induction of CREB‐1 binding to the consensus cyclic AMP‐responsive element. Recombinant IFN‐γ inhibited the BCR‐induced CREB‐1 DNA binding activity and cell proliferation in B cells from signal transducer and activator of transcription‐1 (STAT‐1)+/+, but not STAT‐1–/– mice. These studies provide the first evidence for cross‐talk between the STAT‐1 and CREB‐1 signaling pathways in IFN‐γ‐mediated negative regulation of B cell activation.
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