Search the Community

Celiac.com 09/25/2023 - Professor Jeffrey Hubbell and a team of researchers at the University of Chicago's Pritzker School of Molecular Engineering has developed a novel type of vaccine known as an "inverse vaccine." This innovative vaccine has shown promise in laboratory settings for the treatment of autoimmune diseases such as multiple sclerosis, type 1 diabetes, and Crohn's disease. Importantly, it achieves this without suppressing the entire immune system, as is often the case with current treatments. Could such treatment work for celiac disease? How the Inverse Vaccine Works Traditional vaccines are designed to train the immune system to recognize and attack harmful viruses or bacteria. In contrast, the inverse vaccine takes a different approach. It aims to erase the immune system's memory of a specific molecule. This concept is particularly useful in autoimmune diseases, where the immune system mistakenly attacks the body's healthy tissues. The development of the inverse vaccine is based on the liver's natural mechanism of marking molecules from broken-down cells with signals that instruct the immune system not to attack them. Researchers combined an antigen (a molecule targeted by the immune system in autoimmune diseases) with a molecule resembling a fragment of an aged cell. This mimicry tricks the liver into recognizing the antigen as a friend rather than a foe, effectively stopping the autoimmune reaction. The research team successfully demonstrated the effectiveness of this inverse vaccine in halting autoimmune reactions in a disease model resembling multiple sclerosis. In multiple sclerosis, the immune system attacks myelin, the protective coating around nerves, leading to symptoms such as weakness, numbness, vision loss, and mobility problems. By linking myelin proteins to the molecule recognized by the liver, the researchers were able to prevent the immune system from attacking myelin. This allowed nerves to function properly again, ultimately reversing the disease's symptoms in animal subjects. Importantly, the inverse vaccine approach could have significant advantages over current treatments for autoimmune diseases. Many existing treatments involve broadly suppressing the entire immune system, which can lead to various side effects and increase the risk of infections. In contrast, the inverse vaccine offers a more targeted and specific way to modulate the immune response, potentially minimizing side effects. While further research is needed, initial phase I safety trials have already been conducted in humans with celiac disease, and are underway in multiple sclerosis. These trials are sponsored by the pharmaceutical company Anokion SA, which also contributed to the research. The development of clinically approved inverse vaccines is an exciting prospect, as they could provide more effective and precise treatments for autoimmune diseases, improving the quality of life for patients. Read more at the Pritzker School of Molecular Engineering

Celiac.com 02/03/2023 - Multiple sclerosis is a chronic autoimmune disease of the central nervous system that affects individuals worldwide. People with multiple sclerosis often have other autoimmune diseases such as hypothyroidism, inflammatory bowel disease, rheumatoid arthritis, and diabetes, which suggests that there may be common genetic or environmental exposures between multiple sclerosis and other autoimmune diseases. Epidemiological studies have also shown that individuals with one autoimmune disease have an increased susceptibility to developing another autoimmune disease. Celiac disease is an autoimmune gluten-sensitive enteropathy that results in small intestinal lesions and malabsorption in affected individuals. Celiac disease develops based on genetic factors and mucosal immune response. Almost all individuals with celiac disease have HLA DR3-DQ2 and/or the DR4-DQ8. These HLA class II haplotypes have a strong association with multiple sclerosis. celiac disease is also associated with neurological manifestations and diseases such as ataxia, epilepsy, neuropathy, and multiple sclerosis. However, the exact relationship between celiac disease and multiple sclerosis is not well understood. In order to evaluate the prevalence of celiac disease in multiple sclerosis cases, two researchers conducted a systematic review and meta-analysis using PubMed, Scopus, EMBASE, Web of Science, and Google Scholar. The search included all relevant studies published up to October 2022. The researchers independently searched all databases and also references of included studies. They included cross-sectional studies/case, articles which had been published in the English language, and studies in which the diagnostic criteria were biopsy of the duodenum. They excluded letters to editors, case reports, and RCT studies. They found a total of 1,113 articles by literature search, and after deleting duplicates, 519 remained. Sixteen articles remained for meta-analysis. A total of 31,418 patients were evaluated and the total number of possible/confirmed cases was 124. Studies were published between 2004 and 2020, and the most published studies were from Italy. Five studies provided information regarding controls. The pooled rates of this systematic review showed that celiac disease is not common in multiple sclerosis cases. However, the study did have some limitations. There were studies that used serologic evaluation for celiac disease diagnosis which were excluded. Additionally, there were no reports from some countries, and the control groups were different; as in some studies, the control group was healthy subjects, and in others, the control group was patients with other diseases except multiple sclerosis. The study authors suggest that larger multicenter studies from numerous countries are needed to fully understand the relationship between celiac disease and multiple sclerosis. It is important to note that while the rates of celiac disease in multiple sclerosis patients may be low, patients with multiple sclerosis still suffer from a wide range of gastrointestinal manifestations such as dysphagia, constipation, and/or fecal incontinence. Dyspeptic symptoms and associated pain are also common in multiple sclerosis cases, which can negatively affect quality of life and interfere with daily activities. Because of this, it's important for doctors to be aware of the potential for these symptoms in multiple sclerosis patients, and to consider a range of possible causes. Read more in the American Journal of Gastroenterology

Celiac.com 05/16/2020 - Yes, I’m “just a vet,” but I have realized something very important. If MDs studied veterinary medicine like I have studied human medicine, we would be a lot further down the road toward solving many medical puzzles. For instance, dogs get multiple sclerosis (MS). We call it degenerative myelopathy. It occurs primarily in large breed dogs, with German Shepherds being the number one victim. In fact, the condition in the dog is so similar to that in people that it was once thought that humans may have contracted it from dogs. (As canine distemper virus is a paramyxovirus, and with measles and mumps being paramyxoviruses, such transmission may be possible, especially when we see that many viruses that afflict humans are harbored in animals). If the distemper virus is causing it, why do such a small, select number of dogs get it? Why don’t we see it across the board in all breeds? If it were a parasite (which is highly unlikely), then the same would be true... it should not select the specific breeds. Thus, since genetic traits are specific to breeds, we have to look at “genetics”. But what are “genetics”? They are basically two things- Gene sequences that determine traits and body functions and sequences derived from viruses. Yes, approximately 45% of the genetic information in our DNA is from viruses. This is a very important “fun fact”. The DNA IS “command central.” It contains both the information for normal development and the potential for things to go wrong. Researchers have tried to nail down the “genetics” of MS for a long time but it just doesn’t seem to be working out for them. That’s because MS is complicated and multiple factors have to come together to make it happen. What do we know, other than it happens in select breeds of dogs and that MDs think there is a hereditary link but can’t seem to prove it? M.S. occurs most prevalently in northern climates, above the 33rd parallel. Why? Relative lack of vitamin D, with the consequent lack of sunlight exposure being the main culprit, is the accepted theory. I think they are right. Vitamin D is crucial for the immune system to function properly. A recent medical study boldly proclaimed that if all Americans took an effective vitamin D supplement, we would cut the cancer risks by over a 1/3. Air pollution, which is horribly neurotoxic and immune suppressive, also has a major detrimental effect on MS patients. It does sound like an immune system problem (weakness) doesn’t it? So, what is being unleashed by this weakened immune system? A parasite? (Not likely...we would have SEEN that microscopically long ago. Also, parasites would not be nearly so selective.). A bacteria? ( For the same reasons, this isn’t likely either. A virus? Ahhh...maybe. But why haven’t researchers been able to culture it or at least identify it yet? Perhaps because it is already in the DNA, as is suggested by the limited number of breeds of dogs that are afflicted? We know this happens in the case of retroviruses and cancer. What we also know is that there are some viruses that require “helper” viruses that provide essential amino acid sequences that are missing in the genetic make-up of the primary virus or segment already in place in the DNA. This is well established. Imagine someone who has that incomplete sequence in their DNA then contracts a virus that supplies the missing information. It is like someone putting the right code into a stalled computer....suddenly it starts running. This would help explain the relatively uncommon incidence of MS in both species as well as the “genetic” tendency that investigators just can’t seem to find. It would also explain the demise of the immune system, nutrition, the northern climate prevalence (the vitamin D connection), and just about every other loose end that we have before us right now. With this kind of “idiopathic condition” (MS, epilepsy, Alzheimer’s, Parkinson’s, etc.) we should be looking for a “syndrome”...a number of factors that come together that produce a particular range of results. The really cool thing to see is the role that the big “4” foods play in all of this. Just add the potentially cataclysmic effects of the malabsorption syndrome that goes along with the intolerance (to gluten, casein, soy, corn, which dominate our diet) the direct effect of lectins on cellular function, and the role of viruses, both overt and those whose information is already embedded in our very genome. We need to study all we can about these three things: food intolerance; lectins, and; viruses. If we do, the world of medicine will open up before us. It becomes readily apparent that bacteria, parasites, and fungi/yeast are secondary players. They are opportunists that arise and cause problems as this process unfolds. In fact, I look at them as the clues that can help us understand what is missing - our immune system and microscopic damage done to our tissues. Once we examine them in this way, then we can see them as warning signs to go along with the other signs that preceded their arrival, such as heartburn, IBS, allergies, asthma, chronic fatigue, insomnia, etc. etc.

Celiac.com 01/08/2020 - Researchers currently don't have much good information on the frequency of hypogammaglobulinemia (Ig deficiency) in people with multiple sclerosis. A team of researchers recently set out to assess the frequency of reduced immunoglobulin (Ig) concentrations and its association with immunotherapy and disease course in two independent multiple sclerosis study groups. The research team included Greta Zoehner, Andrei Miclea, Anke Salmen, Nicole Kamber, Lara Diem, Christoph Friedli, Maud Bagnoud, Farhad Ahmadi, Myriam Briner, Nazanin Sédille-Mostafaie, Constantinos Kilidireas, Leonidas Stefanis, Andrew Chan, Robert Hoepner, and Maria Eleftheria Evangelopoulos. The team's retrospective cross-sectional study included multiple sclerosis patients and control patients with head or neck pain from Bern University Hospital in Bern, and Eginition University Hospital in Athens. The lower limits of normal (LLN) for serum Ig concentration were IgG < 700 mg/dl, IgM < 40 mg/dl, and IgA < 70 mg/dl. The team analyzed the results using the Mann–Whitney U test, analysis of variance test, and multiple linear regression. The study shows that multiple sclerosis patients have high rates of reduced serum IgG concentrations, both with and without disease-modifying treatments. Interestingly, in patients with other autoimmune diseases, Ig deficiency is also more prevalent, and 1.7% of patients with celiac disease and 5.2% of patients with systemic lupus erythematosus also have IgA deficiency. Given that infections or interference with antibody production usually happen at much lower IgG levels, around 400 mg/dl, and below, the importance of lower IgG concentrations at the levels noted remains unknown. The team suggests using the information to monitor IgG levels, particularly with anti-B-cell therapies, and considering IgG substitution at levels below 400 mg/dl. Read more in Therapeutic Advances in Neurological Disorders The researchers are variously affiliated with the Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; the University Institute of Clinical Chemistry, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; the Center of Laboratory Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; the Department of Neurology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; and the Department of Neurology, Eginition University Hospital at the National and Kapodistrian University of Athens, Athens, Greece.

Celiac.com 03/25/2019 - Some researchers have suspected that myelin proteins may be involved in multiple sclerosis (MS). A recent report in Science and Translational Medicine, suggests that additional non-myelin-related protein may also play a role. Researchers examined protein samples from the brains of 31 people who had died from suspected or confirmed MS. They found that T cells from 12 people reacted to the enzyme guanosine diphosphate-L-fucose synthase, or GDP-L-fucose-synthase. The enzyme usually helps to process sugars that are crucial to cell function and communication, including the function and communication of neurons. Researcher Dr Roland Martin, from the University Hospital of Zurich, Switzerland, has helped to figure out which myelin proteins and peptides come under attack in MS, and which cells and immune molecules do the attacking. Paper coauthor Mireia Sospedra, of University Hospital of Zurich, suggests that “other auto-antigens might be involved in initiating the disease." She believes that the attack on this newly identified auto-antigen triggers tissue damage that exposes other myelin proteins that are likely targets for attack. Sospedra suspects that some variations in myelin protein structure might be susceptible to immune attack, and that genetic variation in immune cells might influence the body’s response to a given infection. She suggests that the offending antigens may differ between individuals, as the structure of our molecular machinery is genetically determined. Northwestern University immunology professor Stephen Miller, who did not work on this research, but has worked with Dr. Martin in the past, suggests that there’s likely not just “one particular virus or bacteria or environmental factor that triggers MS in every patient. There are probably many things that can trigger an autoimmune reaction against a particular infection," he says. "But the more antigens we identify that can contribute to the disease, the better." Researchers have pointed out that numerous autoimmune diseases seem to cluster in certain gene sequences. Multiple gene areas seem to correlate with numerous autoimmune conditions. Prior comprehensive genetic association studies have found 90 genetic areas associated with T1DM, celiac disease, multiple sclerosis, and/or rheumatoid arthritis. Celiac disease and MS sufferers share some things in common, including a tendency to develop rosacea. Rosacea is a common inflammatory skin condition that shares the same genetic risk location as autoimmune diseases such as type 1 diabetes mellitus (T1DM) and celiac disease. The connections between multiple sclerosis and celiac disease is a common topic of discussions on many forums. Read more at: medscape.com

Celiac.com 08/30/2017 - The human gut is home to a huge and diverse number of microorganisms that perform various biological roles. Disturbances in a healthy gut microbiome might help to trigger various inflammatory diseases, such as multiple sclerosis (MS). Human gut-derived commensal bacteria suppress CNS inflammatory and demyelinating disease. Can they improve the treatment of multiple Sclerosis (MS)? A team of researchers recently set out to evaluate evidence that gut commensals may be used to regulate a systemic immune response and may, therefore, have a possible role in treatment strategies for multiple Sclerosis. The research team included Ashutosh Mangalam, Shailesh K. Shahi, David Luckey, Melissa Karau, Eric Marietta, Ningling Luo, Rok Seon Choung, Josephine Ju, Ramakrishna Sompallae, Katherine Gibson-Corley, Robin Patel, Moses Rodriguez, Chella David, Veena Taneja, and Joseph Murray. In a recent article, the team reports on their identification of human gut-derived commensal bacteria, Prevotella histicola, which can suppress experimental autoimmune encephalomyelitis (EAE) in a human leukocyte antigen (HLA) class II transgenic mouse model. P. histicola suppresses disease through the modulation of systemic immune reactions. P. histicola challenge caused a reduction in pro-inflammatory Th1 and Th17 cells and an increase in CD4+FoxP3+ regulatory T cells, tolerogenic dendritic cells, and suppressive macrophages. This study indicates that gut commensals may regulate a systemic immune response, and so may have a role in future treatments for multiple Sclerosis, and possibly other autoimmune diseases such as celiac disease. Source: Cell.com. DOI: http://dx.doi.org/10.1016/j.celrep.2017.07.031