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Showing results for tags 'immune-mediated'.
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Celiac.com 10/23/2024 - Cardiovascular diseases, such as coronary artery disease and stroke, have long been connected with various immune-mediated disorders due to the role inflammation plays in both conditions. This study explores whether there is a genetic connection between cardiovascular diseases and specific immune-mediated diseases, with a particular focus on psoriasis. Psoriasis is a chronic inflammatory condition that has previously been associated with an increased risk of cardiovascular disease. However, it is unclear whether the genetic risk factors for cardiovascular disease are also linked to an increased risk of psoriasis and other immune-related conditions. Study Objectives The main goal of the study was to investigate whether genetic predispositions to coronary artery disease and stroke also increase the risk of developing psoriasis or other immune-mediated diseases. The researchers utilized a method called Mendelian randomization, which uses genetic data to determine whether there is a causal relationship between two traits, as opposed to just an observed association. By using large datasets from genome-wide association studies, the study aimed to uncover whether genetic predictors of cardiovascular disease are directly linked to immune-mediated diseases, such as psoriasis, rheumatoid arthritis, and inflammatory bowel disease. Methods and Data To conduct the analysis, the study used Mendelian randomization to evaluate the genetic links between cardiovascular disease and immune-mediated diseases. This approach is particularly effective in differentiating causality from correlation because it uses genetic markers as proxies for risk factors. The researchers analyzed summary data from genome-wide association studies for coronary artery disease, stroke, psoriasis, and nine other immune-mediated diseases. The data included a large sample of participants, with over 1.1 million individuals for cardiovascular disease traits and nearly 500,000 for psoriasis. The study specifically examined whether genetic markers associated with coronary artery disease and stroke were linked to an increased risk of developing psoriasis or any of the other immune-mediated diseases. Key Findings The results of the study revealed that genetic predictors for both coronary artery disease and stroke were significantly associated with an increased risk of psoriasis. In particular, genetic risk factors for coronary artery disease were found to increase the risk of developing psoriasis by about 7%, while genetic risk factors for stroke increased the risk by 22%. Interestingly, when adjustments were made for stroke risk, the association between coronary artery disease and psoriasis became statistically insignificant. This suggests that there may be a shared genetic component that links both cardiovascular diseases and psoriasis, rather than two separate pathways. On the other hand, the study found no significant genetic link between cardiovascular disease risk factors and other immune-mediated diseases, such as rheumatoid arthritis and inflammatory bowel disease. This finding was somewhat unexpected, as these diseases also involve inflammation, which is thought to be a common factor in both cardiovascular disease and immune-mediated disorders. Genetic Risk and Celiac Disease The study also explored the relationship between genetic predictors of cardiovascular disease and various immune-mediated diseases, including celiac disease. Data from 4,533 cases of celiac disease and 10,750 controls were included in the analysis. The results indicated no significant association between genetic risk factors for cardiovascular disease—such as coronary artery disease or stroke—and the risk of developing celiac disease. This finding suggests that while cardiovascular genetic factors may influence the risk of developing psoriasis, they do not appear to have the same effect on celiac disease or other immune-mediated conditions. Understanding the Relationship Between Psoriasis and Cardiovascular Disease The discovery that genetic risk factors for cardiovascular disease are linked specifically to psoriasis, but not to other immune-mediated diseases, points to the possibility of a unique shared biological mechanism. Psoriasis is a disease driven by inflammation, and inflammation is also a key factor in the development of cardiovascular diseases like coronary artery disease and stroke. However, the study’s findings suggest that this connection may not extend to all immune-mediated diseases, challenging previous assumptions about the broad relationship between cardiovascular disease and inflammation-driven conditions. One possible explanation for this connection could lie in the specific inflammatory pathways involved in both cardiovascular disease and psoriasis. Psoriasis is known to involve certain inflammatory cellular and cytokine pathways, and these same pathways may play a role in the development of cardiovascular disease. However, these pathways may not be as significant in other immune-mediated diseases, which could explain the lack of genetic association with conditions like rheumatoid arthritis and inflammatory bowel disease. Implications for Treatment and Future Research The findings of this study have several important implications. First, they highlight the need for further research into the shared genetic mechanisms underlying cardiovascular disease and psoriasis. Understanding these mechanisms could lead to the development of new treatments that target both conditions. For example, therapies that reduce inflammation in psoriasis patients could potentially help lower their risk of cardiovascular disease, and vice versa. Second, the study underscores the importance of personalized medicine. As more is learned about the genetic links between different diseases, it becomes increasingly possible to develop tailored treatments that address an individual's unique genetic risk factors. For patients with psoriasis who are also at risk for cardiovascular disease, this could mean more targeted interventions that address both conditions simultaneously. Implications for Those with Celiac Disease The study’s findings highlight the importance of understanding the genetic overlap between cardiovascular disease and psoriasis, but they also underline the distinction when it comes to celiac disease. For those with celiac disease, the results are reassuring as they show no genetic link between cardiovascular risks and the condition. This separation emphasizes that while shared inflammatory pathways may exist between certain immune-mediated diseases and cardiovascular disease, celiac disease does not appear to be influenced by these cardiovascular genetic factors. As such, this research may provide a better understanding of how different immune-mediated diseases interact with cardiovascular health, guiding future research and treatment strategies. Read more at: jamanetwork.com
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- cardiovascular disease
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Celiac.com 02/28/2022 - Immune regulation is important for carcinogenesis; however, the cancer risk profiles associated with immune-mediated diseases, like celiac disease, are not well understood. A team of researchers recently set out to assess the profiles of cancer risk associated with 48 immune-mediated diseases with the risk of total and individual cancers. They also assessed the prospective association of organ-specific immune-mediated diseases with the risk of local and extra-local cancers. The research team included Ming-ming He, MD; Chun-Han Lo, MD, MPH; Kai Wang, MD, PhD; Georgios Polychronidis, MD; Liang Wang, MD; Rong Zhong, PhD; Markus D. Knudsen, PhD; Zhe Fang, MD; and Mingyang Song, MD, ScD. For their prospective cohort study, the team used data from the UK Biobank cohort study on adults aged 37 to 73 years who were recruited at twenty-two assessment centers throughout the UK between January 1, 2006, and December 31, 2010, with follow-up through February 28, 2019. After adjusting for various potential confounders using time-varying Cox proportional hazards regression, the team assessed the connection between immune-mediated diseases with risk of cancer with multivariable hazard ratios (HRs) and 95% CIs. They used the contrast test method to assess heterogeneity in the associations of organ-specific immune-mediated diseases with local and extra-local cancers. In this group study of nearly half a million participants, the team found that immune-mediated diseases were associated with an increased total cancer risk. Organ-specific immune-mediated diseases showed higher associated risk of local cancers than extra-local cancers, and many immune-mediated diseases were associated with increased risk for cancer in the near and distant organs or other systems. Organ-specific immune-mediated diseases had stronger associations with risk of local cancers than extralocal cancers. The associations for individual immune-mediated diseases were largely organ specific, but were also seen for some cancers in the near and distant organs or different systems. Their findings suggest that immune-mediated diseases are associated with risk of cancer at the local and systemic levels, which supports the role of local and systemic immunoregulation in the development of cancers. Read more in JAMA Oncology The researchers are variously affiliated with the Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; the Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston; the Division of Gastroenterology, Massachusetts General Hospital, Harvard Medical School, Boston; the Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany; the Study Centre of the German Surgical Society, University of Heidelberg, Heidelberg, Germany; the Center of Gastrointestinal Surgery, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; the Section for Colorectal Cancer Screening, Cancer Registry of Norway, Oslo, Norway; the Division of Surgery, Department of Transplantation Medicine, Inflammatory Diseases and Transplantation, Norwegian PSC Research Center, Oslo University Hospital, Oslo, Norway; and the Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
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Celiac.com 05/16/2016 - A number of epidemiological and clinical studies suggest a connection between inflammation and Alzheimer disease, their relationship is not well understood and may have implications for treatment and prevention strategies. A research team recently set out to figure out if a subset of genes involved with increased risk of inflammation are also associated with increased risk for Alzheimer disease. The research team included JS Yokoyama, Y Wang, AJ Schork, WK Thompson, CM Karch, C Cruchaga, LK McEvoy, A Witoelar, CH Chen, D Holland, JB Brewer, A Franke, WP Dillon, DM Wilson, P Mukherjee, CP Hess, Z Miller, LW Bonham, J Shen, GD Rabinovici, HJ Rosen, BL Miller, BT Hyman, GD Schellenberg, TH Karlsen, OA Andreassen, AM Dale, RS Desikan; and the Alzheimer’s Disease Neuroimaging Initiative. They are variously affiliated with the Departments of Neurosciences, Cognitive Sciences, Psychiatry, and Radiology at the University of California, San Diego, La Jolla, the Departments of Neurology, Radiology and Biomedical Imaging at the University of California, San Francisco, the Department of Psychiatry, Washington University, St Louis, Missouri, the Division of Mental Health and Addiction, Oslo University Hospital, the Norwegian Centre for Mental Disorders Research, Institute of Clinical Medicine, University of Oslo, the Division of Gastroenterology, and the Norwegian PSC Research Center and KG Jebsen Inflammation Research Centre, Research Institute of Internal Medicine, Division of Cancer Medicine, Surgery and Transplantation at Oslo University Hospital Rikshospitalet, Oslo, Norway, the Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany, the Department of Neurology, Massachusetts General Hospital, Boston, and the Department of Pathology and Laboratory Medicine at the University of Pennsylvania Perelman School of Medicine, Philadelphia. Using data from numerous genome-wide association studies from several clinical research centers, the team conducted a genetic epidemiology study in July 2015, in which they systematically investigated genetic overlap between Alzheimer disease (International Genomics of Alzheimer's Project stage 1) and Crohn's disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, celiac disease, and psoriasis. The team assessed P values and odds ratios from genome-wide association studies of more than 100, 000 individuals from previous comparisons of patients vs respective control groups. They used consensus criteria to confirm diagnosis for each disorder previously made in the parent study. The main outcome was the pleiotropic (conjunction) false discovery rate P value. Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer's Disease Assessment Scale cognitive subscale scores as a measure of cognitive dysfunction (Alzheimer's Disease Neuroimaging Initiative); and gene expression in Alzheimer disease vs control brains (Gene Expression Omnibus data). These findings confirm genetic overlap between Alzheimer disease and immune-mediated diseases, and suggest that immune system processes influence Alzheimer disease pathogenesis and progression. For more detail, and exact data results, see JAMA Neurol. 2016 Apr 18. doi: 10.1001/jamaneurol.2016.0150.
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Celiac.com 12/28/2015 - Immune-mediated cerebellar ataxias include gluten ataxia, paraneoplastic cerebellar degeneration, GAD antibody associated cerebellar ataxia, and Hashimoto's encephalopathy. Despite the identification of an increasing number of immune-mediated cerebellar ataxias, there is no proposed standardized therapy. Recently, a research team set out to develop guidelines for treatment of immune-mediated cerebellar ataxias. The research team included H. Mitoma, M. Hadjivassiliou, and J. Honnorat. They are variously associated with the Department of Medical Education at Tokyo Medical University in Tokyo, Japan; the Academic Department of Neurosciences at Royal Hallamshire Hospital, Sheffield, UK; the University Lyon 1; INSERM, UMR-S1028, CNRS, UMR-5292, Lyon Neuroscience Research Center, Neuro-Oncology and Neuro-Inflammation Team, 7; and the National Reference Centre for Paraneoplastic Neurological Diseases, Hospices Civils de Lyon, Hôpital neurologique in Bron, France. For their study, the team evaluated the efficacies of immunotherapies in reported cases using a common scale of daily activity. Their resulting analysis focuses on the importance of removing autoimmune triggers (e.g., gluten or cancer), evaluating immunotherapy (e.g., corticosteroids, intravenous immunoglobulin, immunosuppressants), and adjusting according to each sub-type. Source: Cerebellum Ataxias. 2015 Nov 10;2:14. doi: 10.1186/s40673-015-0034-y. eCollection 2015.
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- ataxias
- cerebellar
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