Two first-in-class antibodies, C01 and C04, have been developed to inhibit inflammation in autoimmune diseases by blocking the high-affinity IgG receptor FcγRI. The antibodies were discovered using a unique immunization method and exhibit higher affinity for FcγRI than human IgG.
Researchers at Hospital for Special Surgery have uncovered key biological mechanisms driving systemic sclerosis, a rare autoimmune disease that disproportionately affects women. The studies reveal potential treatment targets, including drugs targeting plasmacytoid dendritic cells and CXCL4 cytokine.
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Extracellular vesicles from fibrotic lungs can activate dormant fibroblasts in healthy lungs, initiating fibrosis development and spreading. The study's findings support the potential use of EVs as a targeted drug therapy platform to slow fibrosis progression and improve patient outcomes.
A Phase I/II study found tofacitinib effective in improving skin and organ issues in systemic sclerosis patients. The drug was well-tolerated, with minimal impact on T-cells, suggesting potential repurposing for treatment.
Researchers at Medical University of South Carolina found that scleroderma patients have reduced levels of antifibrotic protein Cathepsin L, packaged in an inactive state. Increasing Cathepsin L levels and function could have therapeutic benefits for patients with lung fibrosis.
A substance produced by gut microorganisms, TMAO, can lead to scarring and vascular damage in scleroderma. The Western diet rich in meat contributes to TMAO formation, which reprograms cells to become scar-forming myofibroblasts.
Researchers at Weill Cornell Medicine discovered that chemokines can form DNA-bound nanoparticles that induce chronic, dysfunctional immune responses. This new mechanism may play a central role in autoimmune diseases such as scleroderma and lupus, where inflammation goes awry.
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A study published in JCI Insight reveals that epigenetic drugs targeting BRD4 significantly reduce scarring in patients with scleroderma. The findings could lead to repurposing these drugs for faster relief from debilitating symptoms of this chronic disease.
A biodegradable nanoparticle has shown promise in reducing skin and lung scarring in mice with scleroderma. The treatment targets specific immune cells responsible for the disease's chronic inflammation and scarring.
Researchers have discovered a new type of skin cell, TIFFs, that may play a role in inflammatory skin diseases such as scleroderma. These cells were found to interact with immune cells and expand in response to inflammation, leading to an exaggerated response and fibrosis.
Researchers discovered a protein called CTRP9 associated with pulmonary function in scleroderma patients with interstitial lung disease. Patients with higher CTRP9 levels developed more severe lung disease, while low levels were linked to preserved function. The study suggests CTRP9 could help predict treatment needs for these patients.
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Researchers found that online mental health intervention improved anxiety and depression in people with scleroderma, a disease causing skin and connective tissue tightening. The four-week program offered group mental health intervention from trained peer support leaders, resulting in significant improvements six weeks later.
Researchers developed an algorithm to screen for pulmonary arterial hypertension in scleroderma patients, outperforming standard methods. The algorithm correctly identified all 10 patients with the condition in a study of 68 subjects.
Researchers found that tocilizumab treatment stabilized forced vital capacity in patients with systemic sclerosis, preventing irreversible lung damage. The study suggests a window of opportunity for select patients to benefit from anti-inflammatory therapy.
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A study published in Cell Reports Medicine found a link between autoantibodies and lung fibrosis progression in systemic sclerosis patients. The researchers discovered that osteopontin, a protein previously implicated in fibrosis, may be responsible for triggering lung scarring.
Researchers at MUSC discover lysyl oxidase plays key roles in promoting fibrosis in scleroderma, and its levels can be used to monitor treatment response. The findings suggest LOX could be a promising biomarker for assessing fibrosis progression or regression.
Researchers at MUSC found that older men with scleroderma have higher estrogen levels than postmenopausal women, which is linked to more severe disease and heart involvement. This discovery provides evidence for the role of estrogen in scleroderma and may lead to new therapeutic approaches.
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Researchers at the University of Leeds have identified a new internal regulator that helps control the body's response to fight infection. The discovery has the potential to help find new drugs to tackle autoimmune diseases, such as lupus and scleroderma, by suppressing the immune system.
Researchers discovered that inhibiting the cancer-causing protein EZH2 can correct increased fibrosis and abnormal blood vessel function in scleroderma patients. This breakthrough suggests that existing EZH2 inhibitors could be repurposed to treat scleroderma, offering new hope for this currently incurable disease.
In scleroderma, IL-6-producing effector B cells promote fibrosis, while IL-10-producing regulatory B cells suppress inflammation. Administering a BAFF antagonist selectively depletes Beffs while sparing Bregs, suggesting this approach could be a therapeutic strategy for SSc.
A new Northwestern Medicine study identified a trigger for some fibrotic diseases and an experimental compound to treat it. The compound, T53, reversed abnormality in three different mouse models of fibrosis, suggesting a novel approach to treat the disease.
A new study finds that the microRNA family miR-17-92 plays a critical role in regulating T-cell and B-cell pathogenicity, leading to chronic graft-vs-host disease. The research also suggests that blocking this miRNA may be an effective way to reduce cGVHD symptoms.
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Rheumatologist Shervin Assassi is developing a blood test to determine which drugs work best for patients with lung disease and scleroderma. The new project aims to create prediction models that identify patients who are likely to respond to immunosuppression.
A new clinical trial has found that a stem cell transplant treatment can significantly improve the survival and quality of life for patients with severe scleroderma. The experimental procedure uses chemotherapy and radiation to destroy the body's malfunctioning immune system, then replaces it via a stem-cell transplant.
A new study by Hospital for Special Surgery researchers suggests that plasmacytoid dendritic cells play a key role in causing fibrosis and inflammation in scleroderma patients. The study's findings, published in Science Translational Medicine, also identify a potential target for treatment: the TLR8 receptor on the surface of these cells.
A new clinical trial has shown that a stem cell transplant regimen can improve survival and quality of life for people with severe scleroderma. The study found myeloablative autologous hematopoietic stem cell transplant to be superior to treatment with the immune-suppressing drug cyclophosphamide, offering significantly greater long-te...
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A new study by Duke University researchers found that stem cell transplant significantly improves survival and reduces the need for immune suppressant drugs in patients with severe scleroderma. The regimen, which includes chemotherapy and radiation, showed a highly significant benefit compared to conventional drug therapy.
Researchers found that low-energy shock-wave therapy significantly reduced digital ulcers in scleroderma patients by stimulating growth factors and forming new blood vessels. The treatment also showed no serious adverse events during the study, making it a promising approach for managing refractory digital ulcers.
Researchers at Hospital for Special Surgery have identified a population of stem cells called ADSCs that are reduced in number in the layer of fat sitting under the skin in patients with scleroderma. The study found that replenishing these cells with antibodies may reverse the fibrosis characteristic of the disease.
A Northwestern University discovery identifies a specific protein, fibronectin (FnEDA), as a key player in promoting fibrosis in people with scleroderma. The study found that blocking this protein's activity can prevent skin fibrosis in mice, offering new avenues for treatment.
Researchers at Michigan State University have identified the core signaling pathway that activates scleroderma and found chemical compounds that can turn it off. This discovery offers a new approach to treating the disease, which currently lacks effective treatments.
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Scientists from the University of Manchester identified Leri's pleonosteosis as caused by extra genetic material on chromosome 8. The condition is also linked to scleroderma and offers opportunities for understanding and treating both diseases.
Researchers found that a cancer trigger may be the cause of autoimmune disease scleroderma, which causes skin thickening and widespread organ damage. The study suggests that dampening down the immune response in scleroderma could instead be replaced by targeting the underlying cancer.
A study at Northwestern University and Dartmouth's Geisel School of Medicine found that patients with improved responses to mycophenolate mofetile (MMF) therapy share a distinct gene expression pattern in skin. This signature can potentially guide targeted treatment for patients with scleroderma.
Researchers at Northwestern University have implicated toll-like receptor 4 (TLR4) in the development of tissue fibrosis, a hallmark of scleroderma. The study found that mutations in the TLR4 gene made mice resistant to experimental scleroderma and that patients with scleroderma had abnormal TLR4 levels in affected tissues.
African-Americans with systemic scleroderma have more antibodies that link to severe complications and increased mortality compared to Caucasians. The study suggests using disease markers to screen and treat patients proactively.
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A genetic pathway previously known for its role in embryonic development and cancer has been identified as a target for systemic sclerosis, or scleroderma, therapy. The finding reveals that the Wnt signaling pathway is abnormally activated in scleroderma patients, leading to fibrosis and tissue damage.
Scleroderma is a chronic autoimmune disease affecting 300,000 US citizens, causing skin thickening and internal organ damage. Researchers at Northwestern will identify biomarkers using proteomics to develop targeted therapies.
A BUSM researcher has received two NIH grants totaling over $11 million to study systemic sclerosis (SSc), a rare and complex rheumatic disease. The funding will support clinical research, molecular studies, and identification of biomarkers to accelerate the understanding of SSc and develop new treatments.
Research identified demographic, clinical, and psychosocial factors contributing to work disability in systemic scleroderma. Findings suggest that retraining and additional support can help individuals with the disease maintain or regain employment.
A Phase II trial of Gleevec (imatinib) has shown acceptable safety and tolerability, with hints of efficacy in treating diffuse scleroderma. The drug improved skin scores by 22% and forced vital capacity scores by 6.4% after 12 months of therapy.
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A new Georgetown University Medical Center study found that up to 40% of scleroderma patients will not be correctly diagnosed using a commercial screening test. The researchers evaluated over 200 scleroderma patients and found that the test failed to identify patients with specific antibodies, highlighting the need for alternative test...
Researchers have found a potential link between autoimmune disease scleroderma and cancer in certain patients. The study suggests that patients with specific immune markers are more likely to develop both conditions simultaneously.
A new genetic link to systemic sclerosis has been identified in a study published in Nature Genetics. The research found that a region of the human genome associated with increased susceptibility to the disease was discovered, which could lead to developing interventions to block its activity.
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A study by Johns Hopkins Medicine reveals that a rare inherited disorder called stiff skin syndrome shares genetic similarities with the debilitating condition scleroderma, affecting about one in 5,000 people. The findings suggest a potential treatment strategy involving the protein fibrillin-1 and its role in regulating TGFbeta activity.
Researchers have discovered a connection between gene expression and the development of lung disease in scleroderma patients. The study suggests that a specific gene profile may predict which individuals are at risk of developing lung complications, providing potential targets for new treatments.
Researchers have identified a drug that could provide the first treatment for scleroderma, a chronic connective tissue disease. In a study of 30 patients with diffuse scleroderma, Gleevec improved skin scores by 23% and lung function tests by 9.6% after one year.
Two studies identified a novel biomarker for metastatic bladder cancer and discovered stem cell factor's role in airway remodeling in asthma. Additionally, researchers found that Staphlococcus aureus beta-toxin causes lung injury in pneumonia, while rosiglitazone may reduce the severity of scleroderma.
Researchers at UT Health Science Center aim to identify genetic clues to scleroderma by studying the genes of 1,500 patients and 3,000 controls. The goal is to develop better treatments and improve symptoms for those affected by this chronic disease.
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Researchers identified four distinct molecular subtypes in patients with scleroderma, offering new hope for better diagnosis and targeted therapies. The study uses gene expression patterns to classify patients, which could help predict disease progression and treatment response.
Researchers at the University of Granada have developed a new system to diagnose pulmonary hypertension earlier. The system uses ultrasound technology and measures pulmonary artery systolic pressure, allowing doctors to identify the condition before it becomes irreversible.
Survival rates for individuals with scleroderma have increased by 12% over the past 30 years, from 54% to 66%, thanks in part to advancements in treatment. Newer medications such as ACE inhibitors have dramatically improved outcomes for patients, particularly in reducing renal crisis mortality.
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A randomized clinical trial has proven that a drug can slow down deterioration of lung function in scleroderma patients. Participants who received treatment had a small but statistically significant improvement in lung function and less shortness of breath compared to those who were not treated.
A new nationwide study found that cyclophosphamide improved breathing, lung function, quality of life, functional disability, and skin thickness in patients with scleroderma. The findings will help researchers develop new drug therapies and better understand the disease's development.
A study by Galina Bogatkevich and colleagues found that the amount of antifibrotic glycoprotein HGF was reduced in African-American scleroderma patients compared to Caucasians. This malfunction may explain the greater severity and worse prognosis for African-Americans with pulmonary fibrosis/scleroderma.
Researchers discovered that paclitaxel can suppress TGF-beta activity and reduce fibrotic tissue formation in scleroderma. The study also found enhanced angiogenesis in scleroderma skin samples, suggesting a potential treatment pathway.
A new study has found that cyclophosphamide significantly improves lung function and reduces breathlessness in patients with scleroderma lung disease. The treatment also reported increased energy levels and functional ability compared to the placebo group.
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Researchers have identified over 2,700 genes with unusual activity in people with scleroderma, a mysterious skin disease. The study's findings suggest the disease is systemic, not confined to visible skin patches, and may lead to improved diagnosis and targeted treatment options.
Researchers will study cellular changes, immune responses, and collagen production to develop more effective treatments for scleroderma. The NIH grants will complement existing investments in scleroderma research and bring scientists closer to finding treatments for this disease.
The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) has established a national family registry for scleroderma research. The registry will study families with one or multiple cases of the disease to identify genetic factors, environmental triggers, and susceptibility genes.
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