IFN-γ-mediated inhibition of antigen receptor-induced B cell proliferation and CREB-1 binding activity requires STAT-1 transcription factor

Frank Frissora; Hue Chen Chen; Joan Durbin; Subbarao Bondala; Natarajan Muthusamy

doi:10.1002/eji.200323657

IFN-γ-mediated inhibition of antigen receptor-induced B cell proliferation and CREB-1 binding activity requires STAT-1 transcription factor

Frank Frissora, Hue Chen Chen, Joan Durbin, Subbarao Bondala, Natarajan Muthusamy

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

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.

Original language	English (US)
Pages (from-to)	907-912
Number of pages	6
Journal	European Journal of Immunology
Volume	33
Issue number	4
DOIs	https://doi.org/10.1002/eji.200323657
State	Published - Apr 1 2003
Externally published	Yes

All Science Journal Classification (ASJC) codes

Immunology and Allergy
Immunology

Keywords

B cell proliferation
CREB-1
IFN-γ
STAT-1

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10.1002/eji.200323657

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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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T1 - IFN-γ-mediated inhibition of antigen receptor-induced B cell proliferation and CREB-1 binding activity requires STAT-1 transcription factor

AU - Frissora, Frank

AU - Chen, Hue Chen

AU - Durbin, Joan

AU - Bondala, Subbarao

AU - Muthusamy, Natarajan

PY - 2003/4/1

Y1 - 2003/4/1

N2 - 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.

AB - 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.

KW - B cell proliferation

KW - CREB-1

KW - IFN-γ

KW - STAT-1

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IFN-γ-mediated inhibition of antigen receptor-induced B cell proliferation and CREB-1 binding activity requires STAT-1 transcription factor

Abstract

All Science Journal Classification (ASJC) codes

Keywords

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