Abstract
Exposure of T cells to inflammatory cytokines leads to phosphorylation-dependent activation of signal transducer and activator of transcription (STAT) 3. T cells from patients with systemic lupus erythematosus (SLE) display increased levels of total and phosphorylated STAT3 which resides primarily in the nucleus. Increased STAT3 is associated with increased expression of target genes. Silencing of STAT3 expression using a small interfering RNA approach resulted in decreased chemokine-provoked SLE T cell migration. Our data suggest that inhibition of STAT3 expression may reverse the signaling aberrations involved in SLE T cell migration.
MeSH terms
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Adult
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Aged
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Cell Adhesion / immunology
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Cell Movement / immunology*
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Chemokines / biosynthesis
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Chemokines / genetics
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Chemokines / immunology*
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Female
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Humans
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Integrins / biosynthesis
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Lupus Erythematosus, Systemic / genetics
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Lupus Erythematosus, Systemic / immunology*
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Lupus Erythematosus, Systemic / metabolism*
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Microscopy, Confocal
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Middle Aged
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Phosphorylation
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RNA, Small Interfering / genetics
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STAT3 Transcription Factor / antagonists & inhibitors
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STAT3 Transcription Factor / biosynthesis*
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STAT3 Transcription Factor / genetics
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STAT3 Transcription Factor / immunology
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T-Lymphocytes / immunology*
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Transcription, Genetic
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Up-Regulation
Substances
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Chemokines
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Integrins
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RNA, Small Interfering
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STAT3 Transcription Factor