NeuroImmunology
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Antibody Assays for Brain Antigens: A New Study Questions Their Utility - YouTube

A recent study reports that the seroprevalence of 25 autoantibodies against brain antigens were found to be comparable for both healthy people and those with...
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T cells engineered to home in on brain cancer

T cells engineered to home in on brain cancer | NeuroImmunology | Scoop.it
Immunotherapies activate T cells to destroy tumours, but the approach has failed in some brain cancers. A strategy to improve migration of T cells across the blood–brain barrier could overcome this limitation.

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JCI Insight - Single-cell RNA sequencing reveals microglia-like cells in cerebrospinal fluid during virologically suppressed HIV

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CNS lymphatic drainage and neuroinflammation are regulated by meningeal lymphatic vasculature

CNS lymphatic drainage and neuroinflammation are regulated by meningeal lymphatic vasculature | NeuroImmunology | Scoop.it
Louveau et al. demonstrate that meningeal lymphatics drain CSF-derived macromolecules and immune cells and play a key role in regulating neuroinflammation. Meningeal lymphatics may represent a new therapeutic target for multiple sclerosis.
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THUR 154 NMDAR-AB encephalitis: frequency of diagnosis and outcomes

THUR 154 NMDAR-AB encephalitis: frequency of diagnosis and outcomes | NeuroImmunology | Scoop.it
Background The association of N-methyl d-aspartate receptor-antibodies (NMDAR-Abs) and encephalitis is now well recognised.

Methods Retrospective review of frequency of diagnosis and outcomes in encephalitis with NMDAR-Abs identified at the Walton Centre between 2012–2017.
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The intestinal barrier in multiple sclerosis: implications for pathophysiology and therapeutics. - The Microbiome

The intestinal barrier in multiple sclerosis: implications for pathophysiology and therapeutics. - The Microbiome | NeuroImmunology | Scoop.it
PubMed ID: 29860380 Camara-Lemarroy CR, Metz L, Meddings JB, Sharkey KA, Wee Yong V Brain. Jul 2018. doi: 10.1093/brain/awy131 COMMENT: This review is focused on the role that the gut microbiome and the intestinal barrier could play in the pathophysiology of multiple sclerosis. In several works it has been reported that some gastrointestinal disorders with intestinal barrier breakdown show evidence of CNS demyelination, probably due to the impact on the functions of CNS microglia that the microbial organisms entering in the circulation provoke. The authors highlight the importance of the intestinal barrier and the mucosal immune cells in the brain-gut axis and describe this host-microbiome interface as a crucial zone of interaction between immune cells and microbial cells: In this review, we describe the intestinal barrier as the physical and functional zone of interaction between the luminal microbiome and the host. Besides its essential role in the regulation of homeostatic processes, the intestinal barrier contains the gut mucosal immune system, a guardian of the integrity of the intestinal tract and the whole organism. Barrier-stabilizing strategies of treatment for multiple esclerosis as probiotics and stabilizers of tight junctions are discussed along the review and proposed as new therapeutic possibilities for multiple esclerosis.   Contributor Raquel Tobes

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ANGLE : Parsortix shows evidence of CTCs in glioblastoma | MarketScreener

ANGLE : Parsortix shows evidence of CTCs in glioblastoma | MarketScreener | NeuroImmunology | Scoop.it
ANGLE plc


PARSORTIX SYSTEM PROVIDES THE FIRST EVIDENCE OF CIRCULATING TUMOUR CELL CLUSTERS IN GLIOBLASTOMA


Parsortix system detects CTCs in...| août 28, 2018...
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https://angleplc.com/wp-content/uploads/British-Journal-of-Cancer-Glioblastoma-01aug18.pdf

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Cerveau et immunité : un dialogue insoupçonné | Pour la Science

Cerveau et immunité : un dialogue insoupçonné | Pour la Science | NeuroImmunology | Scoop.it
La relation entre le cerveau et le système immunitaire ? Inexistante, pensait-on, sauf dans des cas pathologiques. Or on découvre que les deux systèmes sont intimement liés. Une connexion qui aurait une influence sur l’apprentissage et le comportement social.
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Brain tumors trap immune cells needed to fight cancer in the bone marrow, finds research

Brain tumors trap immune cells needed to fight cancer in the bone marrow, finds research | NeuroImmunology | Scoop.it
Certain brain cancers are associated with low numbers of immune system T-cells circulating in the peripheral blood. Low T-cell numbers can be a side-effect of cancer treatment. But it now appears that there is more to the story of these missing T-cells.
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Engrafted parenchymal brain macrophages differ from host microglia in transcriptome, epigenome and response to challenge

Microglia are yolk sac-derived macrophages residing in the parenchyma of brain and spinal cord, where they interact with neurons and other glial cells by constantly probing their surroundings with dynamic extensions. Following different conditioning paradigms and bone marrow (BM) / hematopoietic stem cell (HSC) transplantation, graft-derived cells seed the brain and persistently contribute to the parenchymal brain macrophage compartment. Here we establish that these cells acquire over time microglia characteristics, including ramified morphology, longevity, radio-resistance and clonal expansion. However, even following prolonged CNS residence, transcriptomes and epigenomes of engrafted HSC-derived macrophages remain distinct from yolk sac-derived host microglia. Furthermore, BM graft-derived cells display discrete responses to peripheral endotoxin challenge, as compared to host microglia. Also in human HSC transplant recipients, engrafted cells remain distinct from host microglia, extending our finding to clinical settings. Collectively, our data emphasize the molecular and functional heterogeneity of parenchymal brain macrophages and highlight the clinical implications for patients treated by HSC gene therapy.
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Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease | NeuroImmunology | Scoop.it
Meningeal lymphatic dysfunction promotes amyloid-β deposition in the meninges and worsens brain amyloid-β pathology, acting as an aggravating factor in Alzheimer’s disease and in age-associated cognitive decline; improving meningeal lymphatic function could help to prevent or delay age-associated neurological diseases.

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Regional Distribution of CNS Antigens Differentially Determines T-Cell Mediated Neuroinflammation in a CX3CR1-Dependent Manner

Regional Distribution of CNS Antigens Differentially Determines T-Cell Mediated Neuroinflammation in a CX3CR1-Dependent Manner | NeuroImmunology | Scoop.it
T cells continuously sample CNS-derived antigens in the periphery, yet it is unknown how they sample and respond to CNS antigens derived from distinct brain areas. We expressed ovalbumin (OVA) neoepitopes in regionally distinct CNS areas (Cnp-OVA and Nes-OVA mice) to test peripheral antigen...
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A Tolerogenic Artificial APC Durably Ameliorates Experimental Autoimmune Encephalomyelitis by Directly and Selectively Modulating Myelin Peptide–Autoreactive CD4+ and CD8+ T Cells

A Tolerogenic Artificial APC Durably Ameliorates Experimental Autoimmune Encephalomyelitis by Directly and Selectively Modulating Myelin Peptide–Autoreactive CD4+ and CD8+ T Cells | NeuroImmunology | Scoop.it
In this study, a tolerogenic artificial APC (TaAPC) was developed to directly and selectively modulate myelin-autoreactive CD4+ and CD8+ T cells in the myelin oligodendrocyte glycoprotein (MOG)35–55 peptide–induced experimental autoimmune encephalomyelitis in C57BL/6J mice.

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VCAM1: Gateway to the Aging Brain? | ALZFORUM

VCAM1: Gateway to the Aging Brain? | ALZFORUM | NeuroImmunology | Scoop.it
17 Jul 2018 Remember those eerie research findings evoking “The Twilight Zone”? Mysterious ingredients in the blood of young mice rejuvenated the brains of their elders, while the blood of old mice sped up aging in young’uns. The identity of blood-borne agents of aging remains a mystery, but researchers believe they have at least zeroed in on the agents’ gateway to the brain. At the joint Keystone symposia Advances in Neurodegenerative Disease Research and Therapy / New Frontiers in Neuroinflammation, held June 17–21 in Keystone, Colorado, Tony Wyss-Coray of Stanford University in Palo Alto reported that expression of vascular cell adhesion molecule 1 (VCAM1) on brain endothelial cells was required for old blood to accelerate aging in young brains. In fact, blocking this receptor even slowed classic symptoms of normal brain aging, such as less neurogenesis and more neuroinflammation, in control mice that never received blood transfusions. VCAM1 expression on the luminal side of blood endothelial cells rises with age. VCAM1 expression on the luminal side of blood endothelial cells rises with age. Only with VCAM1 did blood from old mice speed up aging in the brains of young mice. Blood from active mice boosted neurogenesis in sedentary ones. Alkahest started a Phase 2 trial testing a fraction from young human plasma in people with AD. The findings cement the role of systemic factors in brain aging and suggest that blocking their lines of communication with the brain could have restorative effects. The therapeutic prospect is especially appealing because treatments targeting VCAM1 would not need to cross the blood-brain barrier, which remains a formidable hurdle for CNS drug development. The researchers uploaded their findings to BioRxiv, where the pdf has been viewed nearly 2,200 times since January (Yousef et al., 2018).  Aging is the strongest risk factor for Alzheimer’s and most other neurodegenerative diseases. Circulating factors play a key role, according to findings over the years by Wyss-Coray and colleagues. Not only did they find that blood from young mice halted synaptic deficits, loss of neurogenesis, and even memory loss in AD mouse models, but blood from old mice quickened these processes in young mice (Aug 2011 news; May 2014 conference news; Sep 2016 conference news).  At Keystone, Wyss-Coray presented new results of efforts to understand how outside factors manage to drive aging inside the brain. Reasoning that the blood-brain barrier must be an active participant, Wyss-Coray and colleagues sifted through plasma proteomics data the lab had generated in years prior. They searched for proteins whose concentration shot up with age, and which were known to be expressed by the brain endothelial cells (BECs) that line the BBB. Of the 31 proteins that went up with age, eight were expressed in BECs, and five of those were implicated in vascular function. Of those five, soluble VCAM1 stood out as the protein that increased most in the plasma with age, Wyss-Coray reported at Keystone.  VCAM1 Opens Door to Aging. In the young brain, low levels of VCAM1 on brain endothelial cells allow microglia to remain ramified and calm, and neurogenesis to proceed. In the old brain, these cells increase VCAM1 expression, which tethers more leukocytes to their luminal side. This activates microglia, suppresses neurogenesis. [Courtesy of Yousef et al., BioRxiv, 2018.] VCAM1 is part of the immunoglobulin receptor family, whose expression rises on many cell types in response to injury. The receptor binds to the integrin VLA4, expressed on leukocytes. The soluble version of VCAM1—sVCAM1—is continually shed by the ADAM17 protease, and its concentration in the blood correlates with cognitive impairment and even mortality, Wyss-Coray said. To investigate VCAM1 expression on BECs, the scientists infused fluorescently tagged anti-VCAM1 antibodies into mice; this labeled cells expressing the receptor on the luminal side of the cerebrovasculature. They found a patchy, sparse expression pattern. In young mice, at most 4 percent of BECs in hippocampal blood vessels expressed VCAM1, and this rose to about 5 percent as the animals aged. Injecting young mice with lipopolysaccharide boosted VCAM1 expression to 15 percent of BECs, and even more so in older mice. Single-cell RNA sequencing of BECs revealed that VCAM1 expression was limited to BECs in arteries/arterioles and veins/venules; it was not expressed in capillaries. A single-cell transcriptomic study of the brain vasculature, by Christer Betsholtz at Sweden’s Uppsala University, also reported expression of VCAM1 on arteries and veins, but not capillaries (Vanlandewijck et al., 2018).  At Keystone, Wyss-Coray reported that vein/venule BECs expressing VCAM1 also expressed a slew of pro-inflammatory cytokine receptor genes, as well as receptors known to interact with leukocytes. The researchers next investigated how young versus old plasma affected BEC VCAM1 expression. Exposing young mice to plasma from aged mice—whether via parabiosis or intravenous injection—boosted VCAM1 expression on BECs. Similarly, cultured BECs ramped up VCAM1 expression when treated with plasma from old, but not young, mice. Notably, the researchers found the same result when treating young mice or cultured BECs from young mice with aged human plasma. This suggested that shared factors in aged mouse and human plasma ramped up VCAM1 expression on BECs. Stop VCAM1, Stop Aging? Anti-VCAM1 antibodies increase the number of proliferating (EdU+) neural progenitor cells (Sox2+) in the subventricular zone (white lines) of the dentate gyri of young mice treated with aged human plasma (left two panels). Anti-VCAM1 antibodies decrease the number of activated (CD68+) microglia (Iba1+) (right two panels). [Courtesy of Yousef et al., BioRxiv, 2018.] So far so good, but does VCAM1 facilitate what aged plasma does to the brain? To find out, the researchers injected an anti-VCAM1 antibody into young animals treated with plasma from old mice or humans. As seen previously, in young brains, aged plasma reduced proliferation of neural progenitor cells, a marker of neurogenesis, and boosted activation of microglia; however, treatment with the VCAM1 antibody completely blocked these effects. The same was true in the context of normal aging, as 16-month-old mice injected with the antibody every three days for three weeks had higher rates of neurogenesis and fewer reactive microglia than untreated mice. Does the VCAM1 need to be on BECs? To find out, the researchers generated mice in which VCAM1 expression can be shut off only in BECs. Doing so between the age of two and 16 months resulted in old mice having more neurogenesis and less neuroinflammation than did mice that had been expressing VCAM1 on BECs all along. The findings suggest that VCAM1 expression on BECs somehow mediates the detrimental effects of aged plasma on the brain, Wyss-Coray told the audience. It is unclear how this works, but Wyss-Coray hypothesized that systemic factors ramp up VCAM1 expression on the brain endothelium, and possibly also VLA-4 expression on circulating leukocytes. This would lead to leukocyte tethering along the luminal side of the BBB, where they might inflame the endothelium and transmit inflammatory mediators into the brain. Either directly or via activation of microglia, these mediators could suppress neurogenesis. The exact sequence of events remains to be discovered. Fielding questions from the audience after his talk, Wyss-Coray added nuance to his findings. He said that using an anti-VLA4 antibody instead of an anti-VCAM1 antibody prevented the age-related increase in microglial activation but not the decline in neurogenesis. When asked whether a VCAM1 antibody might work as an anti-aging therapeutic, Wyss-Coray cautioned that anti-VLA4 antibodies, which are a standard treatment for people with multiple sclerosis and Crohn’s disease, cause cancer in a small proportion of patients. Given the severity of those diseases, the cancer risk is considered acceptable. “VCAM1 antibodies would probably be seen in a similar light: If they are efficacious against AD or a similar neurodegenerative disease, a black label might be accepted, and the potential cancer risk would be carefully monitored,” he told Alzforum later. Jonas Neher of the German Center for Neurodegenerative Diseases in Tübingen was intrigued by the work. Neher recently reported that systemic inflammation steers the course of future microglial responses to neurodegenerative disease in the brain (Apr 2018 news). However, Neher contends that soluble factors, such as cytokines, are highly likely to play a role in signaling into the brain. Wyss-Coray agreed, adding that soluble factors could still influence the brain via leukocytes, by upregulating both VCAM1 on the endothelium and VLA-4 on leukocytes. ‘Fit’ Infusions, Youthful Fractions While the new data on VCAM1 speak to how old blood ages the brain, the Keystone meeting also featured findings about how young blood, perhaps even that of athletes, rejuvenates. Zurine de Miguel, a senior scientist in Wyss-Coray’s lab, reported that not just youth but physical fitness might bestow neurogenesis powers onto blood. De Miguel found that plasma collected from mice with access to a running wheel and infused into sedentary mice boosted the birth of newborn neurons in them. Previous studies have linked exercise to neurogenesis, and De Miguel’s findings now suggest that factors in the plasma facilitate the benefit. De Miguel also reported that so-called “runner’s plasma” boosted expression of neuroplasticity genes in recipients, and dampened their inflammatory response to lipopolysaccharide. De Miguel demurred when asked to opine whether regular infusions with the blood of exercisers could substitute for actually working out. Eva Czirr of Alkahest, a biotech company in San Carlos, California, presented clinical findings based on Wyss-Coray’s research. He co-founded Alkahest with Karoly Nikolich in hopes of parlaying plasma products into treatments for neurodegenerative and other age-related diseases. The company completed a small Phase 1 study testing the safety of “young plasma” derived from 18- to 22-year-old donors in recipients with mild to moderate AD (Dec 2017 conference news).  As that trial was ongoing, Czirr and colleagues zeroed in on a plasma fraction—dubbed GRF6019—that they speculate will contain the beneficial properties of whole plasma without its downsides. Comprising about 400 proteins, GRF6019 is devoid of immunoglobulins and clotting factors; this eliminates the need to match recipients to donors and reduces the risk of stroke. Plasma fractions are made from pooled plasma of many donors, facilitating production of large, standardized batches. Alkahest acquires its plasma fractions from Barcelona-based Grifols, the world’s largest producer of blood products. Czirr said that Grifols collects an average of 25,000 plasma donations per day around the world. At Keystone, Czirr reported that GRF6019 had lasting benefits in old mice. Three months after receiving intravenous infusions, the mice still had elevated rates of neurogenesis, lower markers of neuroinflammation, and performed better on tests of memory than their untreated counterparts. In addition, Czirr reported that Alkahest’s Phase 2 clinical trial is officially underway (clinicaltrials.gov). The trial tests GRF6019 in 40 participants with clinically diagnosed mild to moderate AD. They will be equally randomized to receive a low or high dose of GRF6019 intravenously for five consecutive days on the first week of the trial, then again for five days during week 13. The primary outcome measure is safety; cognitive, functional, and neuropsychological tests make up secondary outcomes. Participants will be monitored for a total of six months during the trial.—Jessica Shugart REFERENCES News Citations Paper Alert: Do Blood-Borne Factors Control Brain Aging? 31 Aug 2011 In Revival of Parabiosis, Young Blood Rejuvenates Aging Microglia, Cognition 5 May 2014 Young Blood a Boon for APP Mice 14 Sep 2016 Stuck in the Past? Microglial Memories Dictate Response to Aβ 19 Apr 2018 Blood, the Secret Sauce? Focus on Plasma Promises AD Treatment 14 Dec 2017 Therapeutics Citations Young Plasma GRF6019 Paper Citations Vanlandewijck M, He L, Mäe MA, Andrae J, Ando K, Del Gaudio F, Nahar K, Lebouvier T, Laviña B, Gouveia L, Sun Y, Raschperger E, Räsänen M, Zarb Y, Mochizuki N, Keller A, Lendahl U, Betsholtz C. A molecular atlas of cell types and zonation in the brain vasculature. Nature. 2018 Feb 14; PubMed. External Citations Yousef et al., 2018 clinicaltrials.gov) FURTHER READING No Available Further Reading
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Neuroinflammation in Alzheimer's disease

Neuroinflammation in Alzheimer's disease | NeuroImmunology | Scoop.it
Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted
to the neuronal compartment, but includes strong interactions with immunological mechanisms
in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and...
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The irresistible CCL17: New role for the allergy driver: It influences signal transmission in the brain

The irresistible CCL17: New role for the allergy driver: It influences signal transmission in the brain | NeuroImmunology | Scoop.it
Doctors have long known that a high level of the protein CCL17 in the body indicates an allergic reaction. Now scientists have discovered a completely new function: CCL17 also influences signal transmission in the brain.
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Microglial signatures and their role in health and disease

Microglial signatures and their role in health and disease | NeuroImmunology | Scoop.it
Microglia are the primary innate immune cells in the CNS. In the healthy brain, they exhibit a unique molecular homeostatic ‘signature’, consisting of a specific transcriptional profile and surface protein expression pattern, which differs from that of tissue macrophages. In recent years, there have been a number of important advances in our understanding of the molecular signatures of homeostatic microglia and disease-associated microglia that have provided insight into how these cells are regulated in health and disease and how they contribute to the maintenance of the neural environment.

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Neuro-Compass.education | A Multiple Sclerosis Online Resource

Neuro-Compass.education | A Multiple Sclerosis Online Resource | NeuroImmunology | Scoop.it
Neuro-Compass.education is a free, comprehensive, practical medical resource developed by healthcare professionals for healthcare professionals involved in the care of multiple sclerosis.

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A homing system targets therapeutic T cells to brain cancer

A homing system targets therapeutic T cells to brain cancer | NeuroImmunology | Scoop.it
Therapeutic T cells bearing ligands engineered to optimize adhesion and transmigration through the blood–brain barrier can be targeted to brain tumours.
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Novo, Oxford Uni set to launch diabetes alliance and research labs - PharmaTimes

Novo, Oxford Uni set to launch diabetes alliance and research labs - PharmaTimes | NeuroImmunology | Scoop.it
Novo Nordisk and the University of Oxford are poised to begin ground-breaking work on therapeutic targets for type II diabetes with new research facilities set to open next week.- News - PharmaTimes...
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Enhanced TLR2 responses in multiple sclerosis - Fujiwara - - Clinical & Experimental Immunology - Wiley Online Library

Enhanced TLR2 responses in multiple sclerosis - Fujiwara - - Clinical & Experimental Immunology - Wiley Online Library | NeuroImmunology | Scoop.it
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Gene therapy for neurological disorders: progress and prospects

Gene therapy for neurological disorders: progress and prospects | NeuroImmunology | Scoop.it

Adeno-associated viral (AAV) vectors are a rapidly emerging gene therapy platform for the treatment of neurological diseases. In preclinical studies, transgenes encoding therapeutic proteins, microRNAs, antibodies or gene-editing machinery have been successfully delivered to the central nervous system with natural or engineered viral capsids via various routes of administration. Importantly, initial clinical studies have demonstrated encouraging safety and efficacy in diseases such as Parkinson disease and spinal muscular atrophy, as well as durability of transgene expression. Here, we discuss key considerations and challenges in the future design and development of therapeutic AAV vectors, highlighting the most promising targets and recent clinical advances.



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First FDA-approved study of focused ultrasound to open blood-brain barrier

First FDA-approved study of focused ultrasound to open blood-brain barrier | NeuroImmunology | Scoop.it
In the first such clinical trial in the United States, physician-scientists with the University of Maryland School of Medicine (UMSOM) are investigating the use of MRI-guided focused ultrasound to open the blood-brain barrier. The trial will be conducted with patients undergoing brain cancer surgery at the University of Maryland Medical Center (UMMC).
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Dimethyl fumarate therapy suppresses B cell responses and follicular helper T cells in relapsing-remitting multiple sclerosis - Rikke Holm Hansen, Helene Højsgaard Chow, Finn Sellebjerg, Marina Rod...

Dimethyl fumarate therapy suppresses B cell responses and follicular helper T cells in relapsing-remitting multiple sclerosis - Rikke Holm Hansen, Helene Højsgaard Chow, Finn Sellebjerg, Marina Rod... | NeuroImmunology | Scoop.it
In summary, these data suggest an anti-inflammatory role of DMF and its metabolite MMF on the B cell compartment.

Keywords Multiple sclerosis, dimethyl fumarate, B cells, cytokines, follicular helper T cells
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Multiple Sclerosis Research: Oligoclonal bands: what are they doing?

Multiple Sclerosis Research: Oligoclonal bands: what are they doing? | NeuroImmunology | Scoop.it
A blog on multiple sclerosis research...

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