Release date: 2017-06-30 This issue brings you the relevant research progress on the occurrence and treatment of multiple sclerosis. I hope readers can like it. 1. Nat Neurosci: a novel brain injury repair mechanism or can be used to treat multiple sclerosis A recent study has shown that a special type of cell in the immune system plays an important role in the repair of brain damage. This finding has positive implications for the treatment of neurological damage such as multiple sclerosis. The study was made by researchers from Queen's University in Belfast and is considered to be a landmark study revealing the mechanisms of brain damage repair. 2.3 million people worldwide are affected by multiple sclerosis, and this study may help patients get out of the disease. Multiple sclerosis (MS) is a neurological disease common in young people, mainly due to damage to neuronal myelin. In multiple sclerosis, the immune system erroneously attacks the myelin sheath as a heterologous substance, thereby damaging the nervous system of the winter solstice and producing symptoms such as blindness, pain, fatigue, and paralysis. Until now, clinical treatments for multiple sclerosis have been limited to limiting the deterioration of the disease, but it is impossible to repair damaged neurons. A major breakthrough in this recent study was the discovery of the role of immune cells in repairing myelin damage. The findings, published in the most recent issue of "Nature Neuroscience," show that proteins secreted by a class of cells in the immune system are able to target brain stem cells and induce their differentiation to form oligodenocytes due to repair of myelin. The study means that researchers can use this technology to develop a new type of therapy for the treatment of multiple sclerosis. The study's senior author, Dr. Denise Fitzgerald, also suffered from a condition similar to multiple sclerosis, so she had to walk again when she was 21 years old. "This study is important for our understanding of the natural repair of neuronal damage. This not only extends our understanding of the field of neurology, but also has the potential to improve the standard of living of patients with multiple sclerosis." 2. JAMA Neurol: Stem cell transplantation or treatment of multiple sclerosis but how to choose a patient is important A new study suggests that stem cell transplantation may delay disease progression in approximately half of patients with multiple sclerosis, but selecting the right patient is the key to successful treatment. The researchers found that young patients with relapsing multiple sclerosis who had not experienced severe mobility problems and who had no remission from other treatments would achieve better results within five years. But researchers also report that stem cell transplantation can cause death in some patients. "Stem cell transplantation cannot be considered as a cure for multiple sclerosis. But when patients do not respond to other treatments, they can be used as a treatment option for patients with malignant multiple sclerosis," said author Dr. Riccardo Saccardi. Re-launching the immune system using the patient's own stem cells is one way to delay the progression of the disease. However, this approach is also dangerous because the patient's immune system needs to be removed before the transplant is performed. In fact, nearly 3% of patients will die shortly after receiving a transplant, and these deaths are directly related to the transplant. Since multiple sclerosis itself is not life-threatening, these deaths are an important issue to watch. Professor Michael Racke of Ohio State University pointed out that stem cell transplantation is first used in the treatment of some deadly diseases such as leukemia, lymphoma and other cancers. He also said: "There may be some patients with multiple sclerosis who are more suitable for stem cell transplantation, but the process of selecting patients is very important." Professor Racke, author of the study's review, added that a new study comparing stem cell transplantation with other treatments to see if stem cell transplantation is appropriate for patients with multiple sclerosis is about to begin. At present, drugs can delay the progression of multiple sclerosis and help patients control disease symptoms, but there is no cure. To understand how long the patient had undergone stem cell transplantation, the researchers followed up on 281 patients who underwent stem cell transplantation between 1995 and 2006. They found that 46% of patients did not develop disease within five years after transplantation. However, 8 patients (nearly 3%) died within 100 days of transplantation and their death was associated with transplantation. Researchers believe that these deaths may be mainly related to the technology of stem cell transplantation before 2006, and the technology has since been improved. The relevant research results were published in the international academic journal JAMA Neurology. 3. Sci Rep: Breakthrough results! Scientists identify the first blood biomarker to indicate multiple sclerosis Recently, researchers from Macquarie University in Australia have discovered the first blood biomarker to indicate multiple sclerosis (MS), a serious disease that develops in the central nervous system in Australia. It affects about 23,000 people and affects the health of 2.3 million people around the world. Related research published in the international journal Scientific Reports, the findings of which have been the result of 12 years of scientists, the identification of new biomarkers can make researchers identify multiple sclerosis with an accuracy of 85% to 90%; In terms of the disease, tracking the pathogenesis of the disease has been considered to be problematic and time consuming, and a series of experiments are required on the patient, but recent research has shown that simple blood tests can simplify and accelerate scientists. We explore the process of disease pathogenesis. Researcher Gilles Guillemin said that with the support of Dianti MS Pty, we have now developed a new diagnostic kit that will help scientists from around the world to quickly and easily identify patients with multiple sclerosis. This clinical blood test kit can be used within two years, and it also provides some research basis and clues for researchers to develop individualized targeted therapies for the treatment of multiple sclerosis. The results of this study may also have implications for understanding the pathogenesis of other diseases caused by inflammation and neurodegeneration, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, or motor neuron disease. The final researcher, Professor Guillemin concluded that the new detection method itself relies on the detection of compounds in specific biochemical pathways that utilize a molecule called tryptophan, and we all know that tryptophan can participate in brain inflammation. The process that occurs, thus increasing our understanding of the process of cell processing of tryptophan, we may be able to identify the pathogenesis of more types of neurodegenerative diseases. 4. J immunol: Innate immune disorder promotes multiple sclerosis Multiple sclerosis (MS) is a type of malignant central nervous system demyelinating disease, and the causes of such diseases include genetic factors and environmental factors. Since we currently have limited understanding of the pathogenesis of multiple sclerosis, targeted treatments are also limited to targeting T cells and B cells. This type of therapy can effectively inhibit the recurrence of MS, but can not contain the deterioration of MS. Recent studies have shown that LLR2 activator LIPID654 (L654) is present in the circulatory system of healthy people, while L654 is often low in MS patients. Therefore, a decrease in the ligand level of TLR2 may be associated with the onset of MS. In the mouse model of MS (EAE), the study found a significant up-regulation of TLR2 levels in the spinal cord, but the underlying mechanisms are not clear. The severity of the disease was also significantly reduced in the TLR2 deletion mutant mice during MS induction. Since no exogenous adjuvant is added during the experiment, endogenous PAMP or microbial-derived PAMP in mice may be involved in the occurrence and deterioration of the disease. In response to this question, the Robert B. Clark team from the University of Connecticut conducted an in-depth study, and the results were published in the latest issue of the Journal of Immunology. First, the authors stimulated mouse BMDM in vitro using TLR2's natural ligand substance or L654. The results showed that the initial puncturing of BMDM enabled the cells to develop tolerance to TLR2, ie it was no longer sensitive to the second stimulation. Later, the authors established a mouse EAE model and stimulated TLR2, and the results showed that low concentrations of Pam2Cys stimulation can effectively reduce the severity of EAE disease. The authors then further analyzed the tolerance kinetics of TLR2 and found that induction of TLR2 enabled mice to develop tolerance to other TLRs. Finally, the authors found that the tolerance of TLR2 also occurs in the central nervous system and the inflammatory process of the spleen, which they believe is one of the causes of immune tolerance and deterioration of multiple sclerosis. 5. J immunol: new advances in multiple sclerosis research Multiple sclerosis (MS) is a type of chronic autoimmune disease of the central nervous system characterized by damage to the insulating sheath of neurons in the brain or spinal cord. The EAE model of mice is a commonly used animal model for studying multiple sclerosis in humans, in which Th1/Th17 cells can induce demyelination of central nervous cells. Therefore, research using the EAE model can help us develop treatments for multiple sclerosis. Previous studies have found that natural CD4 T cells can at least differentiate into four types of cells: Th1, Th2, Th17 and Treg. Different cell types have intermodulation of cytokines and transcriptional factors, and these activities play an important role in the differentiation of T cell subtypes. The differentiation of certain types of Th cells is inhibited by cytokines produced in other differentiation directions. IL-17 cells have been shown to play a key role in a variety of autoimmune diseases, and the differentiation of native T cells into Th17 cells is dependent on the effects of TGF-b and other pro-inflammatory cytokines. In addition, TGF-b is also able to promote differentiation of peripheral Treg cells. TGF-b is in an unactivated state after synthesis and needs to be cleaved and depolymerized with the LAP polypeptide to release its activity and bind to receptors on the cell surface. Integrins are a class of viscous attachment molecules on the cell surface, composed of two subunits, a and b. So far, a total of 24 integrin subunits have been discovered (18 a and 6 b). Of all the integrin molecules, five contain the av subunit (avb1, avb3, avb5, avb6, avb8) and are capable of binding to specific sequences above the LAP polypeptide in the TGF-b molecule. Therefore, the above five types of integrin molecules may have a certain regulatory effect on the signal of TGF and the differentiation of Th17. In fact, when the cell surface av integrin molecule is knocked out, the differentiation of Th17 cells and the induction of EAE disease are affected. Extracellular matrix protein 1 (ECM1) is a type of 85kd glycosylation protein involved in many processes including physiological regulation of skin, angiogenesis, and tumor progression. However, the role of ECM1 in the immune response is currently limited, and previous studies have found that ECM1 can specifically release from Th2 cells and promote its outward flow from lymph nodes. IL-4 can promote the differentiation of cells into Th2, but at the same time inhibit other types of Th differentiation. Since ECM1 is secreted by Th2 cells, it is possible that ECM1 also inhibits the differentiation of Th17. In response to this problem, the Sun Bing team from the Shanghai Institute of Biological Sciences of the Chinese Academy of Sciences conducted in-depth research, and the results were published in the latest issue of the Journal of Immunology. First, the authors examined the effect of ECM1 protein on the differentiation of Th1/Th17 cells. By intravenous injection of ECM1 recombinant protein and induction of EAE, the authors found that ECM1 treatment can significantly reduce the severity of the disease. Further, the authors found that the differentiation of Th17 cells in the treated mice was significantly inhibited compared with the control mice. . Since the differentiation of Th17 is dependent on the TGF-b signal, the authors hope to know if ECM1 is involved in the signal regulation process of TGF-b. Through in vitro experiments, the authors found that ECM1 protein can inhibit the cleavage and activation of TGF-b, thereby inhibiting the signal transduction of TGF-b. Specifically, ECM1 is capable of binding to av integrin to inhibit TGF-b signaling in DC. Finally, the authors used ECM1-expressing mice to induce EAE and found that IL-17 production was significantly affected. This indirectly demonstrates the negative regulation of ECM1 on Th17 cell differentiation. 6. Sci Rep: Intestinal bacteria or associated with the onset of multiple sclerosis If asked what is wrong with harmful intestinal bacteria, most people may think that harmful intestinal flora can cause digestive problems, such as constipation, flatulence or diarrhea; but scientists have recently discovered that harmful bacteria, or beneficial Insufficient bacterial levels may be directly related to the occurrence of multiple sclerosis, and the study is published in the journal Scientific Reports. Dr. Ashutosh Mangalam said that the human body carries trillions of bacteria in the intestines, commonly known as the gut microbiome. In recent years, several studies have shown that the intestinal flora plays an important role in improving and maintaining human health. Intestinal bacteria are often closely related to the health of the body. For this reason, researchers want to know whether the intestinal flora is directly related to chronic autoimmune diseases, such as multiple sclerosis. At the same time, researchers also want to know whether the body of patients with autoimmune diseases is The gut microbiome is different from the gut microbiome of healthy individuals. The researchers said that in fact, patients with multiple sclerosis have different intestinal microbiota groups than healthy individuals. Although this is a preliminary study, the relevant data indicate that the levels of beneficial bacteria in the body of multiple patients are lower, such as those. A beneficial flora that benefits from healthy foods (soybeans, flax). Researcher Mangalam and researchers from the Mayo Clinic performed microbiological analysis of stool samples from patients with multiple sclerosis, with healthy individuals as controls; the results showed that patients with multiple sclerosis were compared to healthy individuals. The level of specific flora in the body has decreased or increased; in later studies, the researchers said that they will also confirm the findings in this paper by conducting more in-depth studies on a large number of subjects. 7. J Immunol: A new mechanism for the development of multiple sclerosis Multiple sclerosis is a type of chronic autoimmune disease of the central nervous system in which the insulation of neurons in the brain and spinal cord is severely damaged. EAE (mouse meningitis virus model) is a commonly used mouse model for studying multiple sclerosis in humans in which Th1/Th17-mediated autoimmune responses trigger the demyelinating reaction of the central nervous system in mice. Finding out how to control the activation of Th17 has a positive effect on the treatment of human multiple sclerosis. Th17 has an important influence on a variety of autoimmune responses, and natural T cells differentiate into Th17 under the stimulation of TGF-beta and other inflammatory factors. Extracellular matrix protein 1 (ECM1) is a class of 85KD glycosylated proteins involved in the process of skin physiological metabolism, angiogenesis, tumor deterioration and tumor migration. Previous studies have indicated that ECM1 is mainly secreted by Th2 type cells and promotes the migration of Th2 cells from lymph nodes in an asthma disease model. Since IL-4 can promote the differentiation of Th2 cells and inhibit the differentiation of T cells into other directions, ECM1 may play a negative regulatory role in the differentiation of Th17. In order to explore this issue, Sun Bing's research group from Shanghai Institute of Biosciences conducted in-depth research, and the relevant results were published in the latest issue of Journal of Immunology. First, the authors used the mouse EAE model to study and injected ECM1 protein into mice by tail vein injection. The results showed that injection of ECM1 was effective in reducing the severity of EAE disease in mice. Further, the authors found that the differentiation of Th17 cells in ECM1-stimulated mice was affected. However, the number of Th1, Th2, and Treg cells did not change significantly. Through in vitro experiments, the authors found that ECM1 did not inhibit the differentiation of Th17 cells caused by TGF-beta and IL-6, indicating that ECM1 does not directly act on T cells. Later, the authors found that ECM1 inhibits DC secretion of TGF-beta. This indicates that ECM1 further inhibits the differentiation of Th17 by inhibiting the activity of DC. Finally, the authors compared phenotypic differences between wild-type mice and ECM1 overexpressing mice during EAE induction. The results showed that the mutant mice were more tolerant to the induction of EAE. 8. Lancet: New treatments cure multiple sclerosis A new study suggests that a new treatment is expected to cure multiple sclerosis. In a recent clinical trial involving 24 patients in Canada, one patient required a wheelchair condition before treatment and was able to obtain normal life after treatment. However, it should be noted that the degree of the therapy is very severe and one patient died during the treatment. In this regard, the researchers hope to further optimize therapeutic drugs to meet the safety standards for patients with multiple sclerosis. Therapy was discovered by researchers at the Ottawa Hospital Research Institute in Canada, who were treating patients with both leukemia and multiple sclerosis. One of the mainstream methods for treating leukemia is to extract bone marrow cells, kill the remaining immune cells, and then inject the purified bone marrow cells for bone marrow reconstruction. The results show that this reconstructed bone marrow not only helps the treatment of leukemia, but also effectively resists multiple sclerosis. The cause of multiple sclerosis is that immune cells attack the protective tissues of the peripheral nerve cells in the brain, spinal cord, and nervous system. Based on the above results, the researchers decided to conduct a special clinical trial: destroy the immune system and then rebuild it. This treatment is used to prevent the progression of multiple sclerosis, but in most cases it can even completely cure the disease, indicating that the nervous system has a certain ability to heal itself. The clinical trial was conducted in 2000, and 17 out of 24 patients with multiple sclerosis had a significant effect. But this is not a simple treatment, it has serious side effects, so it is only suitable for patients with severe sclerosis. If doctors can find safe optimization methods, it will be a huge improvement. At present, the treatment of multiple sclerosis mainly includes limiting the effects of the disease and reducing the number of acute attacks. Although it cannot solve the problem fundamentally, it is a compromise. Scientists still don't know why the immune system actively attacks nerve cells in multiple sclerosis, but the compromise-reconstruction approach seems to eliminate the memory of the original immune system. The results were published in the journal Lancet. 9. Neuron: Heavy! The first genetic mutation may explain the mystery of the onset of multiple sclerosis Although multiple sclerosis (MS) occurs only in specific families, scientists have repeatedly failed to find genes associated with the disease, and researchers from the University of British Columbia have reported through research. A special genetic mutation, which may be directly related to the pathogenesis of multiple sclerosis, is published in the international journal Neuron. Researcher Carles Vilarino-Guell said that this study is very important for us to understand the pathogenesis of multiple sclerosis. At present, we do not know which biological process leads to multiple sclerosis, and based on this research, scientists They may be expected to develop new therapies for the treatment of multiple sclerosis. Multiple sclerosis is a special neurodegenerative disease in which the immune system attacks the myelin, which protects nerve fibers, and affects the transmission of information between the brain and the body. The disease affects approximately 2 million people worldwide. The health, and currently there are no effective treatments for serious progressive multiple sclerosis scientists. Approximately 10% to 15% of cases of multiple sclerosis have a specific genetic component, but so far, researchers have conducted a large number of genetic studies to find only weak between the onset of multiple sclerosis and specific genetic mutations. Correlation, in comparison, individuals with novel gene mutations may be at risk of 70%. In the current study, the researchers analyzed research materials from the Canadian Multiple Sclerosis Genetic Susceptibility Research Program, which contains genetic material from nearly 2,000 family members in Canada, and researchers who are suffering from multiple sclerosis Conducted a study (two generations, five affected individuals) and performed exome sequencing to find rare coding mutations in the body of all family members. After identifying specific genetic mutations, the researchers The database was re-analyzed and the same genetic mutations were found in other families with multiple sclerosis. More interestingly, all patients in the family who carried the mutation showed progressive multiple sclerosis. . Neuroscientist Weihong Song said that the mutation we found called NR1H3 is a special missense mutation that triggers the loss of gene function, which is the loss of LXRA protein function. LXRA protein can control the transcriptional regulation of specific genes. These genes are mainly involved in the dynamic balance of the body's lipids, inflammation and innate immune function. The researchers point out that mice that knock out the gene often have neurological problems, including a decrease in myelin production, and there is now clear evidence that the mutation can trigger loss of genetic function, and the loss of LXRA protein can also lead to the family. The occurrence of sexual sclerosis. Researcher Carles Vilarino-Guell added that although this novel mutation exists only in one thousandth of the patients with multiple sclerosis, a correlation analysis was performed and the researchers found common mutations in the same gene. Genes are risk factors that trigger the progression of multiple sclerosis; therefore, if there are no rare mutations in the patient's body, therapies that target this pathway may help treat patients with multiple sclerosis. Finally, the researchers say that this study may help develop cell and animal models for the study of multiple sclerosis, and the development of new models may also serve as a research tool to help the pathogenesis of multiple sclerosis in humans, as well as new drug therapies. Development and research. 10. Cell Rep: fasting is beneficial to alleviate autoimmune diseases such as multiple sclerosis A new study suggests that a period of fasting can help fight the development of autoimmune diseases, including lupus erythematosus and multiple sclerosis. Although the study was only targeted at mice, a small human trial later showed that limiting calorie intake did help relieve the symptoms of multiple sclerosis. This result is very satisfactory. “In a fasting-like treatment, the body produces 'cortisone' and kills autoimmune cells,†said lead researcher Valter Longo of the University of Southern California. “This process is accompanied by new healthy cells. produce". So what is the means of fasting? A diet plan like "5:2" (five-days for two days, fasting for two days) or the next-day diet is widely spread, but Longo's new diet plan specifically says: "Three calories a week. Ingestion should be reduced by half." The experimental results of mice and humans have proved that this feeding method can effectively alleviate the body damage caused by autoimmune diseases. Previously, the research team has been studying this field for a long time. They found that proper fasting can not only help reduce weight, but also delay aging and fight disease. "We believe that if this diet can kill a lot of immune cells and initiate differentiation of stem cells, then it might be able to replace the bad part of the cells with good ones," Longo said. To test this hypothesis, they first tested a group of mice with autoimmune diseases. By initiating a fasting diet, they found that the severity of these fasted mice was greater than that of the control group. Significantly alleviated, 20% of the animals were completely recovered. "On the one hand, fasting can kill harmful immune cells. On the other hand, when the mice return to a normal diet, good immune cells begin to form, which makes autoimmune diseases no longer happen." In the next human trial, the researchers recruited 60 patients with multiple sclerosis, some of whom provided a six-month light diet after a week of fasting. The results showed that patients who had undergone fasting treatment had a significant improvement in quality of life, physical and mental health compared with the control group. Combined with mouse-level data, they believe that this result is very satisfactory. The only consideration is that human trials are still at a primary level and limited in scale. If you want to get completely credible conclusions, further research is needed. The relevant results were published in the recent "cell reports" magazine. Source: Bio Valley
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