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151. Effect of Emotional Stimulation on Exercise Heart Rate

Author

Antel, Jack and Cumming, Gordon R.

Abstract

Study supported by the Fitness and Amateur Sport Directorate of Ottawa, and submitted by the senior author for the BSc (Med) degree at the University of Manitoba.

Published
1969

153. A Highly Efficient Human Pluripotent Stem Cell Microglia Model Displays a Neuronal-Co-culture-Specific Expression Profile and Inflammatory Response

Author

Haenseler, Walther; https://orcid.org/0000-0003-4868-3704, Sansom, Stephen N, Buchrieser, Julian, Newey, Sarah E, Moore, Craig S, Nicholls, Francesca J, Chintawar, Satyan, Schnell, Christian, Antel, Jack P, Allen, Nicholas D, Cader, M Zameel, Wade-Martins, Richard, James, William S, Cowley, Sally A, Haenseler, Walther; https://orcid.org/0000-0003-4868-3704, Sansom, Stephen N, Buchrieser, Julian, Newey, Sarah E, Moore, Craig S, Nicholls, Francesca J, Chintawar, Satyan, Schnell, Christian, Antel, Jack P, Allen, Nicholas D, Cader, M Zameel, Wade-Martins, Richard, James, William S, and Cowley, Sally A

Abstract

Microglia are increasingly implicated in brain pathology, particularly neurodegenerative disease, with many genes implicated in Alzheimer's, Parkinson's, and motor neuron disease expressed in microglia. There is, therefore, a need for authentic, efficient in vitro models to study human microglial pathological mechanisms. Microglia originate from the yolk sac as MYB-independent macrophages, migrating into the developing brain to complete differentiation. Here, we recapitulate microglial ontogeny by highly efficient differentiation of embryonic MYB-independent iPSC-derived macrophages then co-culture them with iPSC-derived cortical neurons. Co-cultures retain neuronal maturity and functionality for many weeks. Co-culture microglia express key microglia-specific markers and neurodegenerative disease-relevant genes, develop highly dynamic ramifications, and are phagocytic. Upon activation they become more ameboid, releasing multiple microglia-relevant cytokines. Importantly, co-culture microglia downregulate pathogen-response pathways, upregulate homeostatic function pathways, and promote a more anti-inflammatory and pro-remodeling cytokine response than corresponding monocultures, demonstrating that co-cultures are preferable for modeling authentic microglial physiology.

Published
2017

154. Divergent Neuroinflammatory Regulation of Microglial TREM Expression and Involvement of NF-κB

Author

Owens, Rosie, Grabert, Kathleen, Davies, Claire L., Alfieri, Alessio, Antel, Jack P., Healy, Luke M., and McColl, Barry W.

Subjects
Cellular and Molecular Neuroscience, myeloid cells, TREM2, Correction, microglia, microglial activation, NF-κB, lipopolysaccharide (LPS), Original Research, Neuroscience, neuroinflammation
Abstract

The triggering receptor expressed on myeloid cells (TREM) family of proteins are cell surface receptors with important roles in regulation of myeloid cell inflammatory activity. In the central nervous system, TREM2 is implicated in further roles in microglial homeostasis, neuroinflammation and neurodegeneration. Different TREM receptors appear to have contrasting roles in controlling myeloid immune activity therefore the relative and co-ordinated regulation of their expression is important to understand but is currently poorly understood. We sought to determine how microglial TREM expression is affected under neuroinflammatory conditions in vitro and in vivo. Our data show that microglial Trem1 and Trem2 gene expression are regulated in an opposing manner by lipopolysaccharide (LPS) in vitro in both adult murine and human microglia. LPS caused a significant induction of Trem1 and a contrasting suppression of Trem2 expression. We also observed similar divergent Trem1 and Trem2 responses in vivo in response to acute brain inflammation and acute cerebral ischaemia. Our data show that inhibition of NF-κB activation prevents the LPS-induced alterations in both Trem1 and Trem2 expression in vitro indicating NF-κB as a common signaling intermediate controlling these divergent responses. Distinct patterns of microglial Trem1 induction and Trem2 suppression to different Toll-like receptor (TLR) ligands were also evident, notably with Trem1 induction restricted to those ligands activating TLRs signaling via TRIF. Our data show co-ordinated but divergent regulation of microglial TREM receptor expression with a central role for NF-κB. Neuroinflammatory conditions that alter the balance in TREM expression could therefore be an important influence on microglial inflammatory and homeostatic activity with implications for neuroinflammatory and neurodegenerative disease.

Published
2016

157. A Highly Efficient Human Pluripotent Stem Cell Microglia Model Displays a Neuronal-Co-culture-Specific Expression Profile and Inflammatory Response

Author

Haenseler, Walther, primary, Sansom, Stephen N., additional, Buchrieser, Julian, additional, Newey, Sarah E., additional, Moore, Craig S., additional, Nicholls, Francesca J., additional, Chintawar, Satyan, additional, Schnell, Christian, additional, Antel, Jack P., additional, Allen, Nicholas D., additional, Cader, M. Zameel, additional, Wade-Martins, Richard, additional, James, William S., additional, and Cowley, Sally A., additional

Published
2017
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158. Sublethal oligodendrocyte injury: A reversible condition in multiple sclerosis?

Author

Cui, Qiao-Ling, primary, Khan, Damla, additional, Rone, Malena, additional, T.S. Rao, Vijayaraghava, additional, Johnson, Radia Marie, additional, Lin, Yun Hsuan, additional, Bilodeau, Philippe-Antoine, additional, Hall, Jeffery A., additional, Rodriguez, Moses, additional, Kennedy, Timothy E., additional, Ludwin, Samuel K., additional, and Antel, Jack P., additional

Published
2017
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162. Author Correction: Control of tumor-associated macrophages and T cells in glioblastoma via AHR and CD39

Author

Takenaka, Maisa, Gabriely, Galina, Rothhammer, Veit, Mascanfroni, Ivan, Wheeler, Michael, Chao, Chun-Cheih, Gutiérrez-Vázquez, Cristina, Kenison, Jessica, Tjon, Emily, Barroso, Andreia, Vandeventer, Tyler, Lima, Kalil, Rothweiler, Sonja, Mayo, Lior, Ghannam, Soufiene, Zandee, Stephanie, Healy, Luke, Sherr, David, Farez, Mauricio, Prat, Alexandre, Antel, Jack, Reardon, David, Zhang, Hailei, Robson, Simon, Getz, Gad, Weiner, Howard, and Quintana, Francisco

Abstract

In the version of this article initially published, author Alexandre Prat’s surname was misspelled. The error has been corrected in the HTML and PDF versions of the article.

Published
2024
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163. Clinical course, imaging, and pathological features of 45 adult and pediatric cases of myelin oligodendrocyte glycoprotein antibody-associated disease.

Author

Boudjani, Hayet, Fadda, Giulia, Dufort, Gabrielle, Antel, Jack, Giacomini, Paul, Levesque-Roy, Myriam, Oskoui, Maryam, Duquette, Pierre, Prat, Alexandre, Girard, Marc, Rebillard, Rose-Marie, Meijer, Inge, Pinchefsky, Elana, Nguyen, Cam-Tu Emilie, Rossignol, Elsa, Rouleau, Jacinthe, Blanchard, Oliver, Khairallah, Nicole, Beauchemin, Philippe, and Trudelle, Anne-Marie

Abstract

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently described neuroinflammatory demyelinating disease. To better understand the clinical spectrum, risk factors and outcomes in MOGAD. Retrospective cohort study including all subjects harboring anti-MOG antibodies identified in major academic hospitals across the province of Quebec. We identified 45 MOGAD cases. The minimal estimated point-prevalence was 0.52/100 000 in Quebec. Median age at presentation was 32 years (range 1–71) with equal sex ratio. Most frequent ethnic groups were Caucasians and Asians. The most frequent clinical manifestations at onset were optic neuritis (ON), affecting 56% of adults, and acute disseminated encephalomyelitis (ADEM), affecting 33% of children. First MRI was abnormal in 84% of cases. Most CSF samples showed pleocytosis without oligoclonal bands. Two brain biopsies revealed lipid-laden macrophages and reactive astrocytes. Despite steroids, only 38% had fully recovered at 4 weeks after onset. Half of pediatric and two thirds of adult-onset MOGAD subjects experienced relapses. At last follow-up, 69% showed residual deficits, which were moderate to severe in 17% of adults. MOGAD has heterogeneous disease course, and it is not a benign disease for a substantial proportion of adults. Best disease-modifying therapies remain to be determined. [ABSTRACT FROM AUTHOR]

Published
2023
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169. Glioblastoma-infiltrated innate immune cells resemble M0 macrophage phenotype

Author

Gabrusiewicz, Konrad, primary, Rodriguez, Benjamin, additional, Wei, Jun, additional, Hashimoto, Yuuri, additional, Healy, Luke M., additional, Maiti, Sourindra N., additional, Thomas, Ginu, additional, Zhou, Shouhao, additional, Wang, Qianghu, additional, Elakkad, Ahmed, additional, Liebelt, Brandon D., additional, Yaghi, Nasser K., additional, Ezhilarasan, Ravesanker, additional, Huang, Neal, additional, Weinberg, Jeffrey S., additional, Prabhu, Sujit S., additional, Rao, Ganesh, additional, Sawaya, Raymond, additional, Langford, Lauren A., additional, Bruner, Janet M., additional, Fuller, Gregory N., additional, Bar-Or, Amit, additional, Li, Wei, additional, Colen, Rivka R., additional, Curran, Michael A., additional, Bhat, Krishna P., additional, Antel, Jack P., additional, Cooper, Laurence J., additional, Sulman, Erik P., additional, and Heimberger, Amy B., additional

Published
2016
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170. Effects of fumarates on circulating and CNS myeloid cells in multiple sclerosis

Author

Michell‐Robinson, Mackenzie A., primary, Moore, Craig S., additional, Healy, Luke M., additional, Osso, Lindsay A., additional, Zorko, Nika, additional, Grouza, Vladimir, additional, Touil, Hanane, additional, Poliquin‐Lasnier, Laurence, additional, Trudelle, Anne‐Marie, additional, Giacomini, Paul S., additional, Bar‐Or, Amit, additional, and Antel, Jack P., additional

Published
2015
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171. ISDN2014_0027: REMOVED: Identification of a unique molecular and functional microglia signature in health and disease

Author

Butovsky, Oleg, primary, Jedrychowski, Mark P., additional, Moore, Craig S., additional, Cialic, Ron, additional, Lanser, Amanda J., additional, Gabriely, Galina, additional, Koeglsperger, Thomas, additional, Dake, Ben, additional, Wu, Pauline M., additional, Doykan, Camille E., additional, Fanek, Zain, additional, Liu, LiPing, additional, Chen, Zhuoxun, additional, Rothstein, Jeffrey D., additional, Ransohoff, Richard M., additional, Gygi, Steven P., additional, Antel, Jack P., additional, and Weiner, Howard L., additional

Published
2015
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172. MHC Class I-Restricted Lysis of Human Oligodendrocytes by Myelin Basic Protein Peptide-Specific CD8 T Lymphocytes

Author

Anna Jurewicz, Biddison, William E., and Antel, Jack P.

Subjects
Immunology, Immunology and Allergy
Abstract

Multiple sclerosis (MS) is considered to be an autoimmune disease that is directed either at myelin or at its cell of origin, the oligodendrocytes (OL). The inflammatory lesions in the central nervous system contain multiple myelin Ag-restricted and nonrestricted cell populations with the potential to mediate tissue injury. Previous studies indicate that it is possible to generate MHC class I-restricted myelin peptide-specific cytotoxic CD8 T cells, and that human adult OLs express MHC class I molecules in vitro. The purpose of this study was to demonstrate that myelin basic protein peptide-specific CD8 T cells could induce OL injury. We generated CD8 T cell lines from six healthy donors and five MS patients, and all cell lines were HLA-A2 positive. The obtained CD8 cell lines induced lysis of HLA-A2- but not HLA-A3-transfected HMy2.C1R cells in the presence of myelin basic protein peptide 110–118. In the absence of exogenous peptide, the CD8 T cell lines were cytotoxic to HLA-A2 but not to non-HLA-A2 OLs. Cytotoxicity was blocked with anti-MHC class I-blocking Ab. These results support the postulate that autoreactive CD8 cytotoxic T cells can contribute to the tissue injury in MS.

Published
1998

177. P2Y12 expression and function in alternatively activated human microglia

Author

Moore, Craig S., primary, Ase, Ariel R., additional, Kinsara, Angham, additional, Rao, Vijayaraghava T.S., additional, Michell-Robinson, Mackenzie, additional, Leong, Soo Yuen, additional, Butovsky, Oleg, additional, Ludwin, Samuel K., additional, Séguéla, Philippe, additional, Bar-Or, Amit, additional, and Antel, Jack P., additional

Published
2015
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184. Erratum: Corrigendum: Identification of a unique TGF-β–dependent molecular and functional signature in microglia

Author

Butovsky, Oleg, primary, Jedrychowski, Mark P, additional, Moore, Craig S, additional, Cialic, Ron, additional, Lanser, Amanda J, additional, Gabriely, Galina, additional, Koeglsperger, Thomas, additional, Dake, Ben, additional, Wu, Pauline M, additional, Doykan, Camille E, additional, Fanek, Zain, additional, Liu, LiPing, additional, Chen, Zhuoxun, additional, Rothstein, Jeffrey D, additional, Ransohoff, Richard M, additional, Gygi, Steven P, additional, Antel, Jack P, additional, and Weiner, Howard L, additional

Published
2014
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186. Neuronal progenitors--learning from the hippocampus

Author

Antel, Jack P., Nalbantoglu, Josephine, and Olivier, Andre

Subjects
Central nervous system diseases -- Care and treatment, Central nervous system diseases -- Research, Hippocampus (Brain) -- Health aspects, Hippocampus (Brain) -- Research, Cells -- Transplantation, Cells -- Health aspects, Cells -- Patient outcomes
Abstract

Author(s): Jack P. Antel [1]; Josephine Nalbantoglu [1]; Andre Olivier [1] Successful therapy OF the destructive and degenerative disorders that affect the adult human central nervous system (CNS) will require [...]

Published
2000
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188. Identification of a unique TGF-β–dependent molecular and functional signature in microglia

Author

Butovsky, Oleg, primary, Jedrychowski, Mark P, additional, Moore, Craig S, additional, Cialic, Ron, additional, Lanser, Amanda J, additional, Gabriely, Galina, additional, Koeglsperger, Thomas, additional, Dake, Ben, additional, Wu, Pauline M, additional, Doykan, Camille E, additional, Fanek, Zain, additional, Liu, LiPing, additional, Chen, Zhuoxun, additional, Rothstein, Jeffrey D, additional, Ransohoff, Richard M, additional, Gygi, Steven P, additional, Antel, Jack P, additional, and Weiner, Howard L, additional

Published
2013
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189. Mechanisms goevrning netri-1 induced changes in oligodendroglial morphology during central nervous system development and dysfunction

Author

Kennedy, Timothy E. (Supervisor), Antel, Jack P. (Supervisor), Rajasekharan, Sathyanath, Kennedy, Timothy E. (Supervisor), Antel, Jack P. (Supervisor), and Rajasekharan, Sathyanath

Abstract

Netrin-l is a bifunctional guidance cue that attracts or repels cell of the developing nervous system. Recent work has shown that netrin-l plays important roles in the development of oligodendrocytes, the myelinating cells of the central nervous system (CNS). In the embryonic spinal cord, netrin-l repels dorsally migrating oligodendrocyte precursor cells (OPCs) by inducing a decrease in process extension. In the adult, netrin-l is expressed by mature, myelinating oligodendrocytes and is required for the maintenance ofaxo-oligodendroglial paranodal junctions. This thesis examines a role for netrin-l in oligodendrocyte maturation and during the demyelinating disorder Multiple Sclerosis (MS). I present data demonstrating that netrin-l, acting through its receptor Deleted in Colorectal Carcinoma (DCC), promotes extension and branching of oligodendrocyte processes, and induces the tonnation of myelin-like membrane sheets. These events require the activation of a signal transduction cascade involving the activation of the src-family kinase Fyn and downreb'lllation of GTPbound RhoA. I also explored a mechanism by which netrin-l ellicits contrasting morphological responses in OPCs and oligodendrocytes. Netrin-l increases RhoA activity in OPCs to induce a decrease in process length, but deactivates RhoA to induce process elaboration in oligodendrocytes. The auto immune disease Multiple Sclerosis (MS) is characterized by sporadic CNS demyelination. The last chapter of the thesis identifies the presence of netrin-l, and a proteolytic fragment of netrin-l, in MS lesions. I also detennined that netrin-l induces distinct morphological changes in humanoligodendroglia, and these changes can influence the ability of adult OPCs to efficiently remyelinate a demyelinated lesion. These results indicate that netrin-l plays distinct roles during the orphological maturation of oligodendrocytes, and continues to influence oligodendroglia in the adult CNS, a factor which has important c, La nétrine-l est une molécule de guidage axonal bifonctionnelle qui attire ou repousse les cellules nerveuses ou les axones pendant le développement du système nerveux. Des études récentes ont démontré que la nétrine-l jouc un rôle dans le développement des oligodendrocytes, les cellules productrices de myéline dans le systeme nerveux central (SNC). Dans la moelle épinière embryonnaire, la nétrine-l repousse les précurseurs d' oligodendrocytcs (OPC) dorsalement enprovoquant une réduction de croissance de leur prolongement. Chez l'adulte, la nétrine-l est exprimée par les oligodendrocytes myélinisants matures, et est requise pour le maintien des jonctions paranodales. La présente thèse étudie la fonction de la nétrine-l dans la maturation des oligodendrocytes et son rôle dans la sclérose en plaques (SP), une pathologie démyélinisante du SNC

Published
2009

193. Oligodendrogliopathy in Multiple Sclerosis: Low Glycolytic Metabolic Rate Promotes Oligodendrocyte Survival.

Author

Rone, Malena B., Qiao-Ling Cui, Jun Fang, Li-Chun Wang, Ji Zhang, Khan, Damla, Bedard, Melissa, Almazan, Guillermina, Ludwin, Samuel K., Jones, Russel, Kennedy, Timothy E., and Antel, Jack P.

Subjects
MULTIPLE sclerosis treatment, OLIGODENDROGLIOMAS, OLIGODENDROGLIA, DEMYELINATION, METABOLIC flux analysis
Abstract

Multiple sclerosis (MS) lesions feature demyelination with limited remyelination. A distinct injury phenotype of MS lesions features dying back of oligodendrocyte (OL) terminal processes, a response that destabilizes myelin/axon interactions. This oligodendrogliopathy has been linked with local metabolic stress, similar to the penumbra of ischemic/hypoxic states. Here, we developed an in vitro oligodendrogliopathy model using human CNS-derived OLs and related this injury response to their distinct bioenergetic properties. We determined the energy utilization properties of adult human surgically derived OLs cultured under either optimal or metabolic stress conditions, deprivation of growth factors, and glucose and/or hypoxia using a Seahorse extracellular flux analyzer. Baseline studies were also performed on OL progenitor cells derived from the same tissue and postnatal rat-derived cells. Under basal conditions, adult human OLs were less metabolically active than their progenitors and both were less active than the rat cells. Human OLs and progenitors both used aerobic glycolysis for the majority of ATP production, a process that contributes to protein and lipid production necessary for myelin biosynthesis. Under stress conditions that induce significant process retraction with only marginal cell death, human OLs exhibited a significant reduction in overall energy utilization, particularly in glycolytic ATP production. The stress-induced reduction of glycolytic ATP production by the human OLs would exacerbate myelin process withdrawal while favoring cell survival, providing a potential basis for the oligodendrogliopathy observed in MS. The glycolytic pathway is a potential therapeutic target to promote myelin maintenance and enhance repair in MS. [ABSTRACT FROM AUTHOR]

Published
2016
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194. Effects of fumarates on circulating and CNS myeloid cells in multiple sclerosis.

Author

Michell‐Robinson, Mackenzie A., Moore, Craig S., Healy, Luke M., Osso, Lindsay A., Zorko, Nika, Grouza, Vladimir, Touil, Hanane, Poliquin‐Lasnier, Laurence, Trudelle, Anne‐Marie, Giacomini, Paul S., Bar‐Or, Amit, and Antel, Jack P.

Subjects
BISOPROLOL, MULTIPLE sclerosis, DRUG efficacy, ANTIOXIDANTS, CENTRAL nervous system, MONOCYTES
Abstract

Objective Dimethyl fumarate ( DMF), a therapy for relapsing-remitting multiple sclerosis ( RRMS), is implicated as acting on inflammatory and antioxidant responses within both systemic immune and/or central nervous system ( CNS) compartments. Orally administered DMF is rapidly metabolized to monomethyl fumarate ( MMF). Our aim was to analyze the impact of fumarates on antiinflammatory and antioxidant profiles of human myeloid cells found in the systemic compartment (monocytes) and in the inflamed CNS (blood-derived macrophages and brain-derived microglia). Methods We analyzed cytokine and antioxidant expression in monocytes from untreated or DMF-treated RRMS patients and controls, and in monocyte-derived macrophages (MDMs) and microglia isolated from adult and fetal human brain tissue. Results Monocytes from multiple sclerosis ( MS) patients receiving DMF had reduced expression of the proinflammatory micro- RNA miR-155 and of antioxidant genes HMOX1 and OSGIN1 compared to untreated MS patients; similar changes were observed in patients receiving FTY720 and/or natalizumab. In vitro addition of DMF but not MMF to MDMs and microglia inhibited lipopolysaccharide-induced production of inflammatory cytokines and increased expression of the antioxidant gene HMOX1 in the absence of significant cytotoxicity. Interpretation Our in vivo-based observations that effects of DMF therapy on systemic myeloid cell gene expression are also observed with FTY720 and natalizumab therapy suggests that the effect may be indirect, reflecting reduced overall disease activity. Our in vitro results demonstrate significant effects of DMF but not MMF on inflammation and antioxidant responses by MDMs and microglia, questioning the mechanisms whereby DMF therapy would modulate myeloid cell properties within the CNS. [ABSTRACT FROM AUTHOR]

Published
2016
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197. USP15 regulates type I interferon response and is required for pathogenesis of neuroinflammation

Author

Torre, Sabrina, Polyak, Maria J, Langlais, David, Fodil, Nassima, Kennedy, James M, Radovanovic, Irena, Berghout, Joanne, Leiva-Torres, Gabriel A, Krawczyk, Connie M, Ilangumaran, Subburaj, Mossman, Karen, Liang, Chen, Knobeloch, Klaus-Peter, Healy, Luke M, Antel, Jack, Arbour, Nathalie, Prat, Alexandre, Majewski, Jacek, Lathrop, Mark, Vidal, Silvia M, and Gros, Philippe

Abstract

Genes and pathways in which inactivation dampens tissue inflammation present new opportunities for understanding the pathogenesis of common human inflammatory diseases, including inflammatory bowel disease, rheumatoid arthritis and multiple sclerosis. We identified a mutation in the gene encoding the deubiquitination enzyme USP15 (Usp15L749R) that protected mice against both experimental cerebral malaria (ECM) induced by Plasmodium berghei and experimental autoimmune encephalomyelitis (EAE). Combining immunophenotyping and RNA sequencing in brain (ECM) and spinal cord (EAE) revealed that Usp15L749R-associated resistance to neuroinflammation was linked to dampened type I interferon responses in situ. In hematopoietic cells and in resident brain cells, USP15 was coexpressed with, and functionally acted together with the E3 ubiquitin ligase TRIM25 to positively regulate type I interferon responses and to promote pathogenesis during neuroinflammation. The USP15-TRIM25 dyad might be a potential target for intervention in acute or chronic states of neuroinflammation.

Published
2016
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198. Sphingosine-1-Phosphate Receptors in the Central Nervous and Immune Systems

Author

M. Healy, Luke and P. Antel, Jack

Abstract

Sphingosine-1-phosphate receptor (S1PR) modulators have entered clinical practice as immune-modulators for the treatment of multiple sclerosis (MS). Pharmacologic modulation of S1PR expression on lymphocytes inhibits these cells capacity to respond to the S1P gradient within regional lymph nodes (LNs) (and thymus) that promotes their exit into peripheral circulation. The resultant peripheral blood restricted lymphopenia is considered to underlie the capacity of S1PR modulators to reduce new inflammatory lesion formation in MS in the absence of global immune suppression. These modulators also regulate entry of selective lymphocyte populations and dendritic cells (DCs) into LNs and modulate sphingosine-1-phosphate (S1P) cell signaling networks that govern the generation of specific cell subsets within LNs. S1PR modulators that access the CNS can also have functional effects within this compartment since S1PRs are expressed by cells comprising the blood brain barrier (BBB) and by those within the parenchyma, including neurons, astrocytes, oligodendrocytes and microglia. Absence of S1P1 receptor (S1PR1) on astrocytes reduces disease severity in experimental autoimmune encephalomyelitis (EAE). Even under conditions that inhibit cell responses to the natural ligand, S1PR modulators can continue to induce active signaling responses; such responses may be relevant for promoting neuroprotection and augmenting tissue repair within the CNS.

Published
2016

199. The Tryptophan Metabolite 3-Hydroxyanthranilic Acid Plays Anti-Inflammatory and Neuroprotective Roles During Inflammation

Author

Krause, Daniela, primary, Suh, Hyeon-Sook, additional, Tarassishin, Leonid, additional, Cui, Qiao Ling, additional, Durafourt, Bryce A., additional, Choi, Namjong, additional, Bauman, Avital, additional, Cosenza-Nashat, Melissa, additional, Antel, Jack P., additional, Zhao, Meng-Liang, additional, and Lee, Sunhee C., additional

Published
2011
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