The first human trials are underway to test whether antibody therapy can treat schizophrenia and multiple sclerosis.
NeuroImmunology
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Multiple sclerosis (MS) is a severe disease of the central nervous system (CNS) characterized by autoimmune inflammation and neurodegeneration. 
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Among the wealth of research advances in the field of multiple sclerosis and related disorders in 2015, the following studies shed light on new pathophysiological mechanisms and therapeutic opportunities.
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Exp Ther Med. 2015 Aug;10(2):535-540. Epub 2015 Jun 12.
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Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors.
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Alzheimer’s diseases (AD) and Parkinson’s diseases (PD) are devastating neurodegenerative disturbances, wherein neuroinflammation is a chronic pathogenic process with high therapeutic potential.
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Although the roles of dendritic cells (DCs) in adaptive defense have been defined well, the contribution of DCs to T cell-independent innate defense and subsequent neuroimmunopathology in immune-privileged CNS upon infection with neurotropic...
Krishan Maggon 's curator insight,
December 14, 2015 4:32 AM
Article | OPEN CD11chi Dendritic Cells Regulate Ly-6ChiMonocyte Differentiation to Preserve Immune-privileged CNS in Lethal NeuroinflammationJin Hyoung Kim, Jin Young Choi, Seong Bum Kim, Erdenebelig Uyangaa, Ajit Mahadev Patil, Young Woo Han, Sang-Youel Park, John Hwa Lee, Koanhoi Kim & Seong Kug Eo Scientific Reports 5, Article number: 17548 (2015)doi:10.1038/srep17548Download Citation Published online:02 December 2015
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A 71-year-old woman presented with a 6-week history of progressive involuntary right face and arm jerking movements associated with prominent memory loss and...
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"PTEN deficiency reprogrammes human neural stem cells towards a glioblastoma stem cell-like phenotype" https://t.co/ATF9qwDeib
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The MS Trust looks at some of the issues around stem cell therapy as a possible treatment for multiple sclerosis (MS)
Gilbert C FAURE's insight:
an objective view on the internet
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A new technique, published in Nature Communications, uses lumbar puncture to determine the characteristics of the brain tumour without the need...
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N-methyl-d-aspartate receptor antibody encephalitis: how do we evaluate symptomatic treatment? https://t.co/SIHctal6qa #Neurology
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MS (multiple sclerosis) is a chronic autoimmune disease of the central nervous system characterized by focal demyelination patches associated with inflammatory infiltrates containing T lymphocytes. For decades, CD4+ T cells have been recognized as playing a major role in the disease, especially in animal models, which has led to the development of several therapies. However, interest has recently developed in the involvement of CD8+ T cells in MS following the analysis of infiltrating T cells in human brain lesions. A broad range of evidence now suggests that the pathological role of this T cell subset in MS may have been underestimated. In this review, we summarize the literature implicating CD8+ T cells in the pathophysiology of MS. We present data from studies in the fields of genetics, anatomopathology and immunology, mainly in humans but also in animal models of MS. Altogether, this strongly suggests that CD8+ T cells may be major effectors in the disease process, and that the development of treatments specifically targeting this subset would be germane.
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Neuron. 2015 Dec 10. pii: S0896-6273(15)01030-2. doi: 10.1016/j.neuron.2015.11.024. [Epub ahead of print]
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Research from JAMA Neurology — Combined Plasma and Cerebrospinal Fluid Signature for the Prediction of Midterm Progression From Mild Cognitive Impairment to Alzheimer Disease
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In the past year, several reports have highlighted emerging global threats from neurological infections and have brought up a new appreciation for the particular sensitivity of the CNS to damage from dysregulated inflammatory responses.
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Interleukin-7 is required for CD4+ T cell activation and autoimmune neuroinflammation
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Researchers at the University of Toronto have found another clue in understanding the cause of what drives Multiple Sclerosis (MS) disease. Their findings were published today in Immunity.
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New study showing that in Guillain-Barré syndrome circulating Th17, Th22 cells and Th1 cells are increased along with the plasma levels of IL-17 and IL-22.
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Introduction Foodborne Campylobacter jejuni infection has been associated with an increased risk of autoimmune peripheral neuropathy, but risks of occupational exposure to C . jejuni have received less attention.
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Immune dysfunction is increasingly recognized as a cause of drug-resistant epilepsy but how or why the immune system attacks nerve cells -- and the consequences on seizure control -- are not well understood.
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Pyrvinium Targets CD133 in Human Glioblastoma https://t.co/NX382G12xT #oncology #feedly
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Specific dendritic cells attract autoinflammatory Th17 cells to the CNS in chronic autoimmune diseases https://t.co/1Ro0zn1Rpb AbstractMultiple sclerosis is the most frequent chronic inflammatory disease of the CNS.
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by Gleb Makshakov, Vladimir Nazarov, Olga Kochetova, Elena Surkova, Sergey Lapin, Evgeniy Evdoshenko Background and objective In this study, we evaluated the diagnostic and prognostic significance of cerebrospinal fluid free light chains (CSF FLC)...
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Multiple sclerosis (MS) is mediated primarily by autoreactive T cells. However, evidence suggesting the involvement of humoral immunity in brain diseases has increased interest in the role of B cells and their products during MS pathogenesis. The major survival factor for B cells, BAFF has been shown to play a role in several autoimmune conditions. Elevated BAFF levels have been reported in MS animal model and during MS relapse in patients. Moreover, disease-modifying treatments (DMT) reportedly influence blood BAFF levels in MS patients, but the significance of these changes remains unclear. The present study addresses how blood BAFF levels are associated with the clinical course of relapsing-remitting MS and the effectiveness of DMT and short-term steroid treatment. During a prospective longitudinal follow-up of 2.3 years, BAFF was measured in the blood of 170 MS patients in the stable phase and within 186 relapses. BAFF levels were significantly higher in MS patients compared to healthy controls. However, stable MS patients without relapses exhibited significantly higher BAFF levels than relapsing patients. Treatment with interferon-β and immunosuppressants raised BAFF blood levels. Interestingly, a similar effect was not seen in patients treated with glatiramer acetate. Short-term treatment with high doses of intravenous methylprednisolone did not significantly alter plasma BAFF levels in 65% of relapsing-remitting MS patients. BAFF were correlated weakly but significantly with monocyte and basophil counts, but not with other blood cell types (neutrophils, lymphocytes, or eosinophils) or inflammatory biomarkers. To our knowledge, this is the first report demonstrating that higher blood BAFF levels may reflect a more stable and effective MS treatment outcome. These results challenge hypotheses suggesting that elevated blood BAFF levels are associated with more severe disease presentation and could explain the recent failure of pharmaceutical trials targeting BAFF with soluble receptor for MS treatment.
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B cells in Multiple Sclerosis from Estonia
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