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Mashup Score: 0Activation of gp130 signaling in T cells drives TH17-mediated multi-organ autoimmunity - 10 month(s) ago
Genetic activation of a cytokine receptor in T cells in mice models a STAT3-driven autoimmune syndrome.
Source: www.science.orgCategories: General Medicine News, Cardiologists1Tweet
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Mashup Score: 3Harnessing the regenerative potential of interleukin11 to enhance heart repair - PubMed - 10 month(s) ago
Balancing between regenerative processes and fibrosis is crucial for heart repair 1 . However, strategies to regulate the balance between these two process are a barrier to the development of effective therapies for heart regeneration. While Interleukin 11 (IL11) is known as a fibrotic fa …
Source: pubmed.ncbi.nlm.nih.govCategories: General Medicine News, Cardiologists1Tweet-
My favourite paper so far this year. IL11 essential for fibrosis-mediated (ERK-dependent) heart repair in the zebrafish As predicted…. 😃 https://t.co/fcPFnsz3sC
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Mashup Score: 3
IL6 is a proinflammatory cytokine that binds to membrane-bound IL6 receptor (IL6R) or soluble IL6R to signal via gp130 in cis or trans, respectively. We tested the hypothesis that sgp130Fc, which is believed to be a selective IL6 trans-signalling inhibitor, is in fact a non-specific inhibitor of gp130 signalling. In human cancer and primary cells, sgp130Fc inhibited IL6, IL11, OSM and CT1 cis-signalling. The IC50 values of sgp130Fc for IL6 and OSM cis-signalling were markedly (20- to 200-fold) lower than the concentrations of sgp130Fc used in mouse studies and clinical trials. sgp130 inhibited IL6 and OSM signalling in the presence of an ADAM10/17 inhibitor and the absence of soluble IL6R or OSMR, with effects that were indistinguishable from those of a gp130 neutralising antibody. These data show that sgp130Fc does not exclusively block IL6 trans-signalling and reveal instead that broad inhibition of gp130 signalling likely underlies its therapeutic effects. This proposes global or mo
Source: www.mdpi.comCategories: General Medicine News, Cardiologists1Tweet-
Remember that IL6 trans-signalling thing…well…. Gp130 here we go 👀 https://t.co/D3j9iucqjO
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Mashup Score: 13
Proceeds will fund Phase 2 study in thyroid eye disease (TED) with LASN01 and continue development of LASN500 in Investigational New Drug (IND) enabling studies The Phase 1 study for LASN01 in healthy volunteers has been completed and patient cohorts in idiopathic pulmonary fibrosis (IPF) and TED are enrolling The IND for LASN01 Phase 2 […]
Source: lassentherapeutics.comCategories: General Medicine News, Cardiologists1Tweet-
85 million Anti-IL11 therapy Seems like people now see the potential… 👀 https://t.co/uQk7z0j4NI
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Mashup Score: 10
Interleukin 11 (IL11) is an elusive member of the IL6 family of cytokines. While initially thought to be a haematopoietic and cytoprotective factor, more recent data show instead that IL11 is redundant for haematopoiesis and toxic. In this review, the reasons that led to the original misunderstandin …
Source: pubmed.ncbi.nlm.nih.govCategories: General Medicine News, Cardiologists1Tweet-
A labour of love 218 references 😌 https://t.co/YFxOKooypC
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Mashup Score: 11Fibroblast-derived IL-11 is a driver and therapeutic target in Peutz-Jeghers syndrome polyposis - 1 year(s) ago
Inactivating germline mutations in the tumor suppressor kinase LKB1 (STK11) predispose to Peutz-Jeghers Syndrome (PJS) with increased cancer risk and early-onset development of gastrointestinal polyps requiring regular surveillance. Studies using PJS mouse models have indicated fibroblasts as drivers of polyp formation. Here, we use single-cell RNA sequencing to investigate the fibroblast heterogeneity and tumorigenic mechanisms in a PJS mouse model. We identify five distinct gastric fibroblast subsets, including a polyp-enriched ST2 (Il1rl1)-expressing crypt top fibroblast (CTF) cluster, and show that the polyps arise from Foxl1-expressing CTFs. The transcriptional signature of the ST2-CTFs overlapped with the effects seen by LKB1 loss in vitro and in vivo. The ST2-CTFs also shared similarities with inflammation-associated fibroblasts, and inflammation exacerbated polyposis. Interestingly, the tumorigenic ST2-CTFs showed a distinct signaling pattern, including high expression of inter
Source: www.biorxiv.orgCategories: General Medicine News, Cardiologists1Tweet-
Peutz-Jeghers syndrome - who would have thought it… IL11 pathology is important in a number of rare human genetic diseases: Marfan syndrome Alport syndrome Hermansky-Pudlak syndrome And now PJS Any more? https://t.co/E88qZkXzvA
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Mashup Score: 3
The UK excels at ‘longevity research’. Could it become part of an industry that fascinates the wealthiest people in the world?
Source: www.theguardian.comCategories: General Medicine News, Cardiologists1Tweet-
Too late Try to catch us 😉 https://t.co/lDh54c69kY
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Mashup Score: 1Renal Fibrosis is Alleviated through Targeted Inhibition of Interleukin-11-Induced Renal Tubular Epithelial-to-Mesenchymal Transition - PubMed - 1 year(s) ago
Renal fibrosis is a pathological process that leads to irreversible renal failure without effective treatment. Epithelial-to-mesenchymal transition (EMT) plays a key role in the pathogenesis of renal fibrosis. Herein, we found that tubular aberrant expression of Interleukin (IL)-11 is critically inv …
Source: pubmed.ncbi.nlm.nih.govCategories: Cardiologists1, Latest HeadlinesTweet-
Oh yes! Replicates our findings in CKD and Alport kidney disease and further validates IL11 as a drug target in kidney disease IL11 causes EMT, FMT, EndoMT and VMT - all bad for mammals (good if you are a fish) 👀 https://t.co/3H7jfTOj8O
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Mashup Score: 2SARS-CoV-2 accessory proteins involvement in inflammatory and profibrotic processes through IL11 signaling - 1 year(s) ago
SARS-CoV-2, the cause of the COVID-19 pandemic, possesses eleven accessory proteins encoded in its genome. Their roles during infection are still not completely understood. In this study, transcriptomics analysis revealed that both WNT5A and IL11 were …
Source: www.ncbi.nlm.nih.govCategories: Cardiologists1, Latest HeadlinesTweet-
“increased IL11 led to ECM remodeling. Data from SARS-CoV-2 infected lung cell lines and COVID-19 lung biopsies from patients show a similar response to SARS-Cov-2 infection, so these profibrotic responses may underlie COVID-19-fibrotic alterations” https://t.co/rNDoL4SRXV
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Mashup Score: 0
Chronic liver injury and inflammation triggered by metabolic abnormalities initiate the activation of hepatic stellate cells (HSCs), driving fibrosis and parenchymal dysfunction, culminating in disorders such as nonalcoholic steatohepatitis (NASH). Unfortunately, there are currently no approved drug …
Source: pubmed.ncbi.nlm.nih.govCategories: Cardiologists1, Latest HeadlinesTweet-
Oh the sweet smell of replication: in vivo POC of IL11 as a therapeutic target in NASH (nanoparticles and siRNA used here). Liver scientists not as fast as the lung guys but they got there in the end IPF phase 2s are already planned Liver next? https://t.co/Udg7X7Uyec
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Does this mean that if you block all gp130 signalling you can treat autoimmune disease (not due to germline GOF in STAT3)? If so - SEs permitting- maybe we should try? https://t.co/3CWZgrGoYH