Collectively, these results suggest that LMT-28 can inhibit differentiated/activated-Th17 cells in rheumatoid arthritis by blocking activation of the STAT3 pathway.
The aims of this study were to investigate the effects of IL-17 on the proliferation and autophagy of FLSs and the role of signal transducer and activator of transcription-3 (STAT3) in RA.
We aimed to investigate the immunologic mechanisms by which arsenic trioxide (As<sub>2</sub>O<sub>3</sub>) may inhibit T helper 17 (Th17) cell differentiation while promoting regulatory T (Treg) cell generation by modulating signal transducer and activator of transcription 3 (STAT3) in treatment-naïve rheumatoid arthritis (RA) patients.
Proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocytes following signal transducer and activator of transcription 3 RNA interference delivery.
Ethanolic extract of Kaempferia parviflora interrupts the mechanisms-associated rheumatoid arthritis in SW982 culture model via p38/STAT1 and STAT3 pathways.
Corrigendum: Signal Transducer and Activator of Transcription 3 Hyperactivation Associates With Follicular Helper T Cell Differentiation and Disease Activity in Rheumatoid Arthritis.
Patients harboring STAT3 mutations were more prone to rheumatoid arthritis (4/13 versus 0/15 in the wild-type STAT3 group; P = .04), frequently requiring therapy for neutropenia/neutropenia-associated infections, and demonstrated good therapeutic responses to methotrexate.
Leptin-stimulated RA PBMC upregulated CD4<sup>+</sup>CXCR5<sup>+</sup>ICOS<sup>+</sup> T cells, along with increased IL-6, IL-21, and IL-12.CD4<sup>+</sup>CXCR5<sup>+</sup>ICOS<sup>+</sup> T cells, Bcl-6 mRNA expression, pSTAT1, and pSTAT3 obviously declined when anti-IL-6R antibody was added into leptin-treated RA PBMC, which suggested that leptin upregulated RA CD4<sup>+</sup>CXCR5<sup>+</sup>ICOS<sup>+</sup> T cells via increased IL-6 by activation of STAT1 and STAT3.
From our data, it can be concluded that aspirin is able to promote apoptosis and inhibit the proliferation of RA‑FLS through blocking the JAK/STAT3 and NF‑κB signaling pathways.
Signal Transducer and Activator of Transcription 3 Hyperactivation Associates With Follicular Helper T Cell Differentiation and Disease Activity in Rheumatoid Arthritis.
Thus, administration of the Stat3 inhibitor STA-21 inhibits cellular signaling pathways and downstream activation of key transcription factors previously shown to play key roles in the pathogenesis of RA.
Downregulation of miR-20a promoted the expression of STAT3, p-STAT3, and Bcl-2, facilitated FLS cell proliferation, reduced apoptosis and, thereby, played a critical role in RA.
Ellipticine shows anti-proliferative and pro-apoptotic effects on RA-FLSs through inhibition of the STAT3 pathway and may have therapeutic potential in RA.
Taken together, our findings demonstrate that IL-17 regulates SHP-2 expression and IL-17RA/STAT-3 dependent production of Cyr61, IL-23, GM-CSF and RANKL in AA-FLS and may reveal a new insight into the pathogenesis of RA.
Interleukin 34 Upregulation Contributes to the Increment of MicroRNA 21 Expression through STAT3 Activation Associated with Disease Activity in Rheumatoid Arthritis.