AI Article Synopsis
- Exposure to inflammatory cytokines activates STAT3 in T cells, particularly in those from systemic lupus erythematosus (SLE) patients.
- Increased levels of total and phosphorylated STAT3 in SLE T cells are linked to higher expression of target genes involved in immune response.
- Silencing STAT3 with small interfering RNA reduces T cell migration, indicating that targeting STAT3 might help correct migration issues seen in SLE.
Article 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.
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| http://dx.doi.org/10.1080/08916930601095148 | DOI Listing |
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