HI-Bio: A Biogen Company’s Post

https://lnkd.in/ekkHFWZr Article title: Proximal radial pseudotumour: magnetic resonance imaging appearances and prevalence   Author(s): Ian Pressney; Michael Khoo; Asif Saifuddin Journal: Annals of Bone Marrow Research   Journal ISSN: 2692-4684 Introduction: Cases have been referred to our tertiary referral sarcoma service where marrow abnormalities have been identified in the proximal radius. We believe this to be a normal variant, likely representing residual red marrow. The purpose of this study is to describe the features and determine the prevalence of such a finding on elbow magnetic resonance imaging (MRI) in an unselected group of patients imaged at our institution. #Pseudotumour #Radialtuberosity #Redmarrow #Magneticresonanceimaging #BoneMarrow #BloodSamples #Hematology #AutoimmuneDiseases #StemCells #Immunology #Transplantation #MinimalInvasiveSurgeryTechniques #TranscriptionFactors #Medication #TropicalTreatments #Metabolism #Mortality #DrugTargeting #DrugSensitivity #Resistance #HabitsAndLifestyle #PrognosticFactors #Pathophysiology #NovelDrugs #CellularTherapy #TranslationalResearch #MesenchymalStemCell #HematopoieticStemCellTransplantation #BoneMarrowTransplantation #BoneMarrowEdema #BoneMarrowCancer #BoneMarrowBarrier

#Neuroimmunology | #Neuroinflammation | Endogenous self-peptides guard immune privilege of the #CNS | Major New Paradigm from Jonathan Kipnis and Co. now breaking online #Nature 🧠 | #multiplesclerosis | #autoimmunity | The central nervous system (CNS), despite the presence of strategically positioned anatomical barriers designed to protect it, is not entirely isolated from the immune system. In fact, it remains physically connected to and can be influenced by the peripheral immune system. How the CNS retains such responsiveness while maintaining an immunologically unique status remains an outstanding conundrum. Here*, in searching for molecular cues that derive from the CNS and allow its direct communication with the immune system, researchers discovered an endogenous repertoire of CNS-derived regulatory self-peptides presented on major histocompatibility complex (MHC) II molecules at the CNS borders. During homeostasis, these regulatory self-peptides were found to be bound to MHC II molecules throughout the path of lymphatic drainage from the brain to its surrounding meninges and its draining cervical lymph nodes. With neuroinflammatory disease, however, the presentation of regulatory self-peptides diminished. Upon boosting the presentation of these regulatory self-peptides, a population of suppressor CD4+ T cells was expanded, controlling CNS autoimmunity in a CTLA-4 and TGFβ dependent manner. This unexpected discovery of CNS-derived autoimmune self-peptides may be the molecular key adapting the CNS to maintain continuous dialogue with the immune system while balancing overt autoreactivity. This sheds new light on how we conceptually think about and therapeutically target neuroinflammatory and neurodegenerative diseases. *https://lnkd.in/epkKb8R5 Celentyx Ltd Professor Nicholas Barnes PhD, FBPhS Omar Qureshi Catherine Brady FIGURE | The meningeal & BBBs of the CNS | A coronal brain section is depicted with overlying skull, dura mater, and leptomeninges (arachnoid mater & pia mater) | From Leonel Ampie & Dorian McGavern | https://lnkd.in/en9bG9Cu |

#InnateImmunity in #NeuroDegenerativeDiseases | #Microglia | Focus on #PatternRecognitionReceptors & #DAMPs in Breaking Review from Sergio Castro-Gomez. MD-PhD & Michael Heneka at Cell Press #Immunity 🧠 | Activation of the innate immune system following pattern recognition receptor binding has emerged as one of the major pathogenic mechanisms in neurodegenerative disease. Experimental, epidemiological, pathological, and genetic evidence underscores the meaning of innate immune activation during the prodromal as well as clinical phases of several neurodegenerative disorders including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and frontotemporal dementia. Importantly, innate immune activation and the subsequent release of inflammatory mediators contribute mechanistically to other hallmarks of neurodegenerative diseases such as aberrant proteostatis, pathological protein aggregation, cytoskeleton abnormalities, altered energy homeostasis, RNA and DNA defects, and synaptic and network disbalance and ultimately to the induction of neuronal cell death. In this review*, the authors discuss common mechanisms of innate immune activation in neurodegeneration, with particular emphasis on the pattern recognition receptors (PRRs) and other receptors involved in the detection of damage-associated molecular patterns (DAMPs). *https://lnkd.in/euRr4nC8 Celentyx Ltd #human #microglia #drugdiscovery #platforms https://lnkd.in/eMWCkkDw Professor Nicholas Barnes PhD, FBPhS Omar Qureshi Jamie Cowley Catherine Brady FIGURE | Innate immune dysfunction in AD | Fibrillar Aβ and aggregated p-tau act as main DAMPs, leading to glial activation and innate immunity responses initially in vulnerable regions of the brainstem and the temporal lobe. Other altered molecules resulting from neurodegenerative processes such as ATP, histones, HMGB1, S100s, and reactive oxygen species (ROS) also activate diverse DAMP-sensing receptors such as TLRs, TREM2, purinergic receptors, cGAS-STING, and inflammasomes, with subsequent production and chronic release of pro-inflammatory cytokines. Microglial cells associated with Aβ plaques also express MHC-II molecules to initiate adaptative immune responses

I am thrilled to share my new publication in the International Journal of MS Care (IJMSC)! Read it here: https://lnkd.in/eAr2jBfM #MSResearch #Neuroimmunology

Multiple sclerosis - adding to our understanding of this disease. A recent publication has found that there appear to be three distinct disease trajectories in MS. Prof Heinz Wiendl and his team from the Department of Neurology, University of Munster, Germany have said that this is a "rationale for precision medicine for the future". MS itself is a complex heterogenous disorder which has made it challenging to manage. In their studies, the team found that the 'cellular immune signatures split into three distinct immunological endophenotypes, dubbed E1, E2 and E3' with each of these subtypes being linked to distinct clinical disease trajectories. Read further ... https://lnkd.in/gyQYHUn7 #multiplesclerosis #MS #newfindings

Did you know that people with aHUS may have medical care led by different specialty fields?   Atypical HUS can be categorized as a hematologic disease, with reduced red blood cell & platelet counts. #aHUS #hematology #nephrology #immunology #TMA #complement #cmTMA 

Our recent paper, presenting the first systematic review of Treg levels in migraine patients, reveals a significant reduction in these cells, suggesting a potential autoimmune connection in migraine pathophysiology. The findings offer valuable insights for future research. Read more: https://lnkd.in/gkY-D_b5 #MigraineResearch #Immunology #MetaAnalysis

💡 A new study led by our member Thomas Korn sheds light on the role of B cells in neuromyelitis optica (NMO), an autoimmune disorder of the central nervous system in which the immune system erroneously targets the AQP4 protein. Korn and his team have uncovered B cells' role: they instruct T cells on their target for attack. 🔗 Read a summary of the publication in Nature on our website: https://lnkd.in/d8pEp_pR #Neuromyelitisoptica #Neuroimmunology

Autoantibodies in Neurological Disease Autoantibodies are antibodies that mistakenly target and react with an individual's own tissues and play a crucial role in the pathogenesis of various neurological diseases. In neurological diseases, these autoantibodies can target proteins, receptors, or ion channels in the central or peripheral nervous system, leading to impaired neurological function. The development of autoantibodies in neurological diseases is often associated with a dysregulation of the immune system. Genetic predisposition, environmental factors, infections, and molecular mimicry can trigger the immune system to produce autoantibodies. Once produced, these antibodies can cross the blood-brain barrier or directly target neural tissue, leading to inflammation and neuronal damage. This process has been implicated in diseases such as multiple sclerosis (MS), where autoantibodies target myelin, and neuromyelitis optica (NMO), where they attack aquaporin-4 channels. Autoantibodies against glutamate receptors or voltage-gated potassium channels have also been associated with autoimmune encephalitis, leading to psychiatric and cognitive symptoms. In many cases, the presence of autoantibodies can serve as a diagnostic marker for specific autoimmune neurological diseases. For example, autoantibodies against acetylcholine receptors are a hallmark of myasthenia gravis, which causes muscle weakness. Although the exact mechanisms of autoantibody production in neurological diseases are not fully understood, ongoing research is aimed at discovering therapeutic strategies to neutralize or inhibit these harmful antibodies. Such interventions have the potential to reduce disease severity and improve patient outcomes. References [1] Harald Pruss, Nature Reviews Immunology 2021 (https://lnkd.in/eDkZ6m9G) #Autoantibodies #NeurologicalDiseases #Immunology #MultipleSclerosis #AutoimmuneDisorders #Neuroimmunology #Therapeutics