PDD2: PSYCHOMETRIC PROPERTIES OF THE PATIENT BENEFIT QUESTIONNAIRE (PBQ) IN A COHORT OF DIABETIC PERIPHERAL NEUROPATHY (DPN) PATIENTS

Modulation of mRNA decay by ER stress is MAPK-independent. (TIF 571 kb

Additional file 2: of Can baseline serum microRNAs predict response to TNF-alpha inhibitors in rheumatoid arthritis?

Baseline characteristics of patients in the discovery and validation cohort, split for received treatment. (DOCX 19 kb

Solanum maximowiczii Koidz.

原著和名: マルバノホロシ科名: ナス科 = Solanaceae採集地: 静岡県 巣雲山 (伊豆 巣雲山)採集日: 1966/9/15採集者: 萩庭丈壽整理番号: JH001157国立科学博物館整理番号: TNS-VS-95115

Additional file 2: Figure S2. of Endoplasmic reticulum stress cooperates with Toll-like receptor ligation in driving activation of rheumatoid arthritis fibroblast-like synoviocytes

ER stress effects on TLR-proximal signaling pathways. (TIF 875 kb

Additional file 4: Figure S4. of Endoplasmic reticulum stress cooperates with Toll-like receptor ligation in driving activation of rheumatoid arthritis fibroblast-like synoviocytes

Modulation of mRNA decay by ER stress is MAPK-independent. (TIF 571 kb

Additional file 6: of Can baseline serum microRNAs predict response to TNF-alpha inhibitors in rheumatoid arthritis?

Clinical parameters at baseline associated with current miRNA levels. Serum values of the four selected miRNAs were tested for their relationship with clinical parameters, independent from response. (DOCX 16 kb

Additional file 2: of Control of cytokine mRNA degradation by the histone deacetylase inhibitor ITF2357 in rheumatoid arthritis fibroblast-like synoviocytes: beyond transcriptional regulation

Figure S2. Effects of ITF2357 on mRNA stability. (PDF 816 kb

Additional file 4: of Control of cytokine mRNA degradation by the histone deacetylase inhibitor ITF2357 in rheumatoid arthritis fibroblast-like synoviocytes: beyond transcriptional regulation

Sequences of primers. (PDF 111 kb

Additional file 1: of Multiplicative interaction of functional inflammasome genetic variants in determining the risk of gout

Association power curves. Figure presenting the power of the genetic association analysis. (PPTX 161 kb

Image_2_IL11-mediated stromal cell activation may not be the master regulator of pro-fibrotic signaling downstream of TGFβ.tif

Fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF) and systemic scleroderma (SSc), are commonly associated with high morbidity and mortality, thereby representing a significant unmet medical need. Interleukin 11 (IL11)-mediated cell activation has been identified as a central mechanism for promoting fibrosis downstream of TGFβ. IL11 signaling has recently been reported to promote fibroblast-to-myofibroblast transition, thus leading to various pro-fibrotic phenotypic changes. We confirmed increased mRNA expression of IL11 and IL11Rα in fibrotic diseases by OMICs approaches and in situ hybridization. However, the vital role of IL11 as a driver for fibrosis was not recapitulated. While induction of IL11 secretion was observed downstream of TGFβ signaling in human lung fibroblasts and epithelial cells, the cellular responses induced by IL11 was quantitatively and qualitatively inferior to that of TGFβ at the transcriptional and translational levels. IL11 blocking antibodies inhibited IL11Rα-proximal STAT3 activation but failed to block TGFβ-induced profibrotic signals. In summary, our results challenge the concept of IL11 blockade as a strategy for providing transformative treatment for fibrosis.</p