17 Cambridge Immunology Forum Neuro-Immunology Queens

Total Page:16

File Type:pdf, Size:1020Kb

17 Cambridge Immunology Forum Neuro-Immunology Queens 17th Cambridge Immunology Forum Neuro-Immunology Queens’ College, Cambridge. 22nd September, 2016 Organisers: Brian Ferguson and Andrew McKenzie Coordinator: Tammy Dougan Programme 08.30 Registration and Coffee 09:15 Welcome Session 1 Chair – Brian Ferguson 09:30 Jonathan Kipnis (USA) Meningeal immunity in CNS function and diseases 10:15 Dorian McGavern (USA) Dynamic insights into the pathogenesis of traumatic brain injury and CNS infections 11:00-11:40 Coffee and Posters Session 2 Chair – Michelle Linterman 11:40 Michael Carroll (USA) Complement C4 as a risk allele for Schizophrenia 12:25 Julia Gibbs (UK) Regulation of inflammatory responses by the circadian clock 13:10 – 14:10 Buffet Lunch and Posters Session 3 Chair – Gillian Griffiths 14:10 Shohreh Issazadeh-Navikas (Copenhagen) Neurons tame T cells & Neuroinflammation; impact on FoxA1+ Regulatory T cell fate 14:55 Alasdair Coles (UK) Treating the inflamed brain 15:40 - 16:15 Coffee and poster winners Session 4 Chair – Andrew McKenzie 16:15 Michal Schwartz (Israel) Immune checkpoint blockade for empowering the immune system to fight against Alzheimer’s disease and dementia The Michael Neuberger Lecture 17:00 Eicke Latz (Germany and USA) Role of inflammasomes in Alzheimer’s Disease pathogenesis 17:45 Close and thanks 18.00 Drinks and Conference Dinner Speaker Biographies Jonathan Kipnis Dr. Jonathan (Jony) Kipnis’s research group focuses on the complex interactions between the immune system and the central nervous system. The goal is to elucidate the cellular and molecular mechanisms underlying the beneficial effects of immune cells in central nervous system (CNS) homeostasis after CNS injury and in chronic neurodegenerative conditions. Dr. Kipnis’s research team showed that the immune cells mediate their beneficial effects on the CNS from within the meningeal spaces. Elimination of meningeal T cells or their produced IL-4 results in cognitive impairment. The fascination with meningeal immunity and its role in healthy and diseased CNS is what brought the team to study immune cell trafficking in and out of this understudied compartment. These studies have recently resulted in a breakthrough discovery of meningeal lymphatic vessels that drain the macromolecules and the immune cells from the cerebrospinal fluid/CNS into the deep cervical lymph nodes. The main focus of the Kipnis lab now is to address the role of meningeal lymphatic vessels in regulation of the immune response and brain drainage in different neuroinflammatory and neurodegenerative diseases. He graduated from the Weizmann Institute of Science in Israel, where he was a Sir Charles Clore scholar. Upon graduation, he received the Prize of Excellence from the Weizmann Institute of Science and a distinguished prize for scientific achievements awarded by the Israeli Parliament, The Knesset. He was awarded the Robert Ader New Investigator Award for 2011 by the PsychoNeuroImmunology Research Society and the 2012 Jordi Folch-Pi award by the American Society for Neurochemistry. In 2015 Jony became a Gutenberg Research College Fellow at the Johannes Gutenberg University Mainz Medical Center and recently he was elected as Harrison Distinguished Teaching Professor of Neuroscience at the University of Virginia. Dorian McGavern Dr. McGavern received his B.S degree in microbiology from The Pennsylvania State University and his Ph.D. in molecular neuroscience from the Mayo Clinic. Following an academic appointment as an Associate Professor in the Department of Immunology and Microbial Sciences at The Scripps Research Institute, Dr. McGavern joined the NINDS in March 2009. Dr. McGavern is the recipient of the prestigious Ray Thomas Edwards Foundation Award and the Burroughs Wellcome Fund Pathogenesis of Infectious Disease Award. His laboratory at the NIH is focused on states of acute and persistent viral infection of the central nervous system (CNS). As Chief of the Viral Immunology and Intravital Imaging Unit, Dr. McGavern investigates the impact of viral infections on the CNS as well as how the innate and adaptive immune systems respond to pathogens in this privileged compartment. Michael Carroll Dr. Carroll received his Ph.D. in Immunology from the UT Southwestern Medical School (Dallas, TX) under the direction of Dr. J. Donald Capra in 1980; subsequently he trained with Dr. Rodney R. Porter in the Biochemistry Department, Oxford University (Oxford UK). In 1985, he was appointed an Assistant Professor in Pediatrics and the Department of Biological Chemistry at the Children’s Hospital/Harvard Medical School. He was promoted in 1998 to the rank of Professor of Pediatrics, Harvard Medical School and Senior Investigator, Boston Children's Hospital, Program in Cellular and Molecular Medicine. Dr. Carroll serves as Director of the PhD Graduate Program in Immunology and co-Director of the Masters in Medical Sciences in Immunology Program at Harvard Medical School. He is the author of over 150 peer -reviewed articles*. Early in his career he was an American Arthritis Foundation Fellow and Investigator (1980-1986) and later a recipient of a Pew Scholar award (1986-90). A major focus of his research is development of genetic mouse models for studying human diseases such as lupus and host protection against infection. Most recently, he has extended the study of complement to learn more about how aberrant expression in the central nervous system can underlie schizophrenia and neuropsychosis in lupus patients. Julia Gibbs Dr Gibbs studied Neuroscience at the University of Manchester before completing her PhD at Kings College London. Following a 2 year post-doctoral position at St George’s University of London, she moved back to Manchester in 2006 where she began working as a post-doctoral research associate in the Loudon laboratory, investigating the role of the lung clock in pulmonary inflammation. Here she established the importance of the pulmonary non-epithelial Club cell in regulating timing within the lung, and became interested in how timers within peripheral tissues regulate localised inflammatory responses. She was awarded a Stepping Stones Fellowship by her Faculty in 2012 and began working on the role of the circadian clock in chronic inflammation. This led to her being awarded an Arthritis Research UK Career Development Fellowship in 2014. After a period of maternity leave in 2014 (to have twin girls) she is now running a lab in the Faculty of Medical and Human Sciences at University of Manchester, and continues to study the influence of the circadian clock on inflammatory disease. Shohreh Issazadeh-Navikas Professor Shohreh Issazadeh-Navikas (SI), Biotech Research and Innovation Centre (BRIC), University of Copenhagen, is the head of Neuroinflammation Unit at BRIC. She is trained biologist, performed her Dr. Med. Sci./PhD in the field of Experimental Neurology at Karolinska institute, Sweden and postdoctoral fellowship at Harvard Medical School, USA. Since 2007, she is a full professor at BRIC, University of Copenhagen. She is well known for her contribution in the field of cytokine regulation and the bi-directional communication between neurons and T lymphocytes in central nervous system (CNS). Her lab has been among the first to identify and describe immunological properties of neurons in the CNS and their impact on regulation of immune cells and brain inflammation. Additionally her lab has identified a new type of T regulatory cells (FoxA1+ Treg cells) essential to limit neuroinflammation. The team also identified the first immune genes (IFN-beta and its receptor IFNAR), lack of which causes Parkinson’s-like pathology and dementia in mice. She has served as scientific chair and advisor of several prestigious research councils in Sweden, Germany, and Israel. She has been acting as an expert/advisor for National Institute of Health, USA. She is regularly acting as reviewer for high ranked, and prestigious journals. Alasdair Coles Alasdair Coles is a neurologist in Cambridge. From 1994, his research with Alastair Compston, led to licensing of alemtuzumab as a highly effective treatment for multiple sclerosis in Europe, United States and 50 other countries; and also its approval by NICE in 2014. He ran the first investigator-led trial in relapsing-remitting multiple sclerosis and was the UK chief investigator of the commercially-sponsored phase 2 and both phase 3 trials. His work not only defined the safety and efficacy of this particular drug but has also demonstrated the importance of using immunotherapy early in the course of the multiple sclerosis. His group has shown that alemtuzumab is immunogenic and demonstrated, in a first-in-human study, a novel strategy to reduce immunogenicity of any biological therapy by inducing “high zone tolerance”. The principal adverse effect of alemtuzumab is autoimmunity and his group has (a) identified serum IL-21 as a predictive biomarker of autoimmunity after alemtuzumab and (b) shown that autoimmunity arises when reconstitution of the immune repertoire after alemtuzumab occurs by homeostatic expansion of residual lymphocytes. This led to a trial of keratinocyte growth factor to promote thymic lymphopoiesis and so prevent autoimmunity after alemtuzumab. Michal Schwartz Michal Schwartz is a Professor of Neuroimmunology, incumbent of The Maurice and Ilse Katz Professorial Chair in Neuroimmunology, at the Weizmann Institute of Science, Rehovot, Israel, and the incoming elected president of the International Society of Neuroimmunology (ISNI) for the years 2016-2018. Schwartz received
Recommended publications
  • Immune Senescence and Brain Aging: Can Rejuvenation of Immunity Reverse Memory Loss?
    Opinion Immune senescence and brain aging: can rejuvenation of immunity reverse memory loss? Noga Ron-Harel and Michal Schwartz Department of Neurobiology, The Weizmann Institute of Science, 76100, Rehovot, Israel The factors that determine brain aging remain a mystery. assisting in its restoration [2–8]. In this article, we suggest Do brain aging and memory loss reflect processes occur- a model that attributes to age-related immune compromise ring only within the brain? Here, we present a novel a role in age-related brain dysfunction and, specifically, in view, linking aging of adaptive immunity to brain senes- hippocampus-dependent memory deterioration. According cence and specifically to spatial memory deterioration. to this view, during old age, when the need for maintenance Inborn immune deficiency, in addition to sudden impo- increases, the senescent immune system fails to provide sition of immune malfunction in young animals, results the support required. The individual onset and rate of age- in cognitive impairment. As a corollary, immune restor- related memory impairments are determined both by the ation at adulthood or in the elderly results in a reversal of baseline of cognitive ability (i.e. intelligence) and the rate memory loss. These results, together with the known of cognitive aging [9]. We suggest that the latter is deter- deterioration of adaptive immunity in the elderly, mined by the subject’s immune potential at old age, in suggest that memory loss does not solely reflect chrono- addition to other known factors including early education logical age; rather, it is an outcome of the gap between and lifelong dietary habits [10–12].
    [Show full text]
  • Spinal Cord Injury: Time to Move?
    11782 • The Journal of Neuroscience, October 31, 2007 • 27(44):11782–11792 Symposium Spinal Cord Injury: Time to Move? Serge Rossignol,1,2 Martin Schwab,3,4 Michal Schwartz,5 and Michael G. Fehlings6 1Department of Physiology and Groupe de Recherche sur le Syste`me Nerveux Central, University of Montreal, Faculty of Medicine, Montreal, Quebec, Canada H3C 3J7, 2Multidisciplinary Team on Locomotor Rehabilitation, Canadian Institutes of Health Research, Ottawa, Ontario, Canada K1A 0W9, 3Brain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland, 4Department of Biology, Swiss Federal Institute of Technology, CH-8092 Zurich, Switzerland, 5Department of Neurobiology, The Weizmann Institute of Science, Rehovot 76100, Israel, and 6University Health Network, University of Toronto, Toronto, Ontario, Canada M5G 2C4 This symposium aims at summarizing some of the scientific bases for current or planned clinical trials in patients with spinal cord injury (SCI). It stems from the interactions of four researchers involved in basic and clinical research who presented their work at a dedicated Symposium of the Society for Neuroscience in San Diego. After SCI, primary and secondary damage occurs and several endogenous processes are triggered that may foster or hinder axonal reconnection from supralesional structures. Studies in animals show that some of these processes can be enhanced or decreased by exogenous interventions using drugs to diminish repulsive barriers (anti-Nogo, anti-Rho) that prevent regeneration and/or sprouting of axons. Cell grafts are also envisaged to enhance beneficial immunological mechanisms (autologous macrophages, vaccines) or remyelinate axons (oligodendrocytes derived from stem cells). Some of these treatments could be planned concurrently with neurosurgical approaches that are themselves beneficial to decrease secondary damage (e.g., decompression/reconstructive spinal surgery).
    [Show full text]
  • 13Th Isni Congress Congress Program
    13TH ISNI CONGRESS CONGRESS PROGRAM SCIENTIFIC PROGRAM DAY 1 – MONDAY 26 – GSNI Morning Session – 09.15-13.00 Chairs: Gianvito Martino, Hugh Willison and V. Wee Yong 09.15-09.30: Introduction to the course 09.30-10.15: Microglia in development and disease (Luca Muzio, Italy) 10.15-11.00: Oligodendrocytes in neuroimmunological disorders (Jack Antel, Canada) 11.30-12.15: Astrocytes as key regulators of neuroinflammation (Francisco Quintana, USA) 12.15-13.00: Neurons in CNS inflammatory disorders (Frauke Zipp, Germany) Afternoon Session – 14.30-18.00 Chairs: Gianvito Martino, Hugh Willison and V. Wee Yong 14.30-15.15: Mitochondria and neuroprotection (Don Mahad, UK) 15.15-16.00: Brain aging and neurodegeneration (Tony Wyss-Coray, USA) 16.30-17.15: Fundamentals of psychoneuroimmunology: implications in neuroimmunological disorders (Asya Rolls, Israel) 17.15-18.00: Viruses in neuroimmunological disorders (Yoshihisa Yamano, Japan) DAY 2 – TUESDAY 27 – ISNI Morning Session – 08.00-13.00 Welcome Address 08.00-08.30 Minister of Health Mayor of Jerusalem V. Wee Yong Michal Schwartz Oded Abramsky – A short history of ISNI Plenary Symposium: 08.30-10.40 Repair/regeneration, stem cells and neuroimmunomodulation Chairs: Catherine Lubetzki and Zaal Kokaia 08.30: Remyelination and demyelinating diseases (Catherine Lubetzki, France) 08.52: Therapeutic plasticity of neural stem cells (Gianvito Martino, Italy) 09.13: Neuronal stem cells: the natural resources for regeneration (Tamir Ben-Hur, Israel) 09.35: Mechanisms of somatic adult stem cells with focus
    [Show full text]
  • Neuroimmunology Research. a Report from the Cuban Network of Neuroimmunology
    behavioral sciences Conference Report Neuroimmunology Research. A Report from the Cuban Network of Neuroimmunology María de los Angeles Robinson-Agramonte 1,*, Lourdes Lorigados Pedre 1 ID and Orlando Ramón Serrano-Barrera 2 ID 1 Neuroimmunology Laboratory, Immunochemical Department, International Center for Neurological Restoration, Ave 25 # 15805 b/w 158 and 160, Playa, Havana 11300, Cuba; [email protected] 2 Las Tunas General Hospital, Post Office Box 27, Las Tunas 75100, Cuba; [email protected] * Correspondence: [email protected]; Tel.: +537-2716-385 Received: 7 March 2018; Accepted: 25 April 2018; Published: 8 May 2018 Abstract: Neuroimmunology can be traced back to the XIX century through the descriptions of some of the disease’s models (e.g., multiple sclerosis and Guillain Barret syndrome, amongst others). The diagnostic tools are based in the cerebrospinal fluid (CSF) analysis developed by Quincke or in the development of neuroimmunotherapy with the earlier expression in Pasteur’s vaccine for rabies. Nevertheless, this field, which began to become delineated as an independent research area in the 1940s, has evolved as an innovative and integrative field at the shared edges of neurosciences, immunology, and related clinical and research areas, which are currently becoming a major concern for neuroscience and indeed for all of the scientific community linked to it. The workshop focused on several topics: (1) the molecular mechanisms of immunoregulation in health and neurological diseases, (like multiple sclerosis,
    [Show full text]
  • Neuronal Survival After CNS Insult Is Determined by a Genetically Encoded Autoimmune Response
    The Journal of Neuroscience, July 1, 2001, 21(13):4564–4571 Neuronal Survival after CNS Insult Is Determined by a Genetically Encoded Autoimmune Response Jonathan Kipnis, Eti Yoles, Hadas Schori, Ehud Hauben, Iftach Shaked, and Michal Schwartz Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel Injury to the CNS is often followed by a spread of damage susceptible strains devoid of mature T-cells (as a result of (secondary degeneration), resulting in neuronal losses that are having undergone thymectomy at birth), the numbers of surviv- substantially greater than might have been predicted from the ing neurons after optic nerve injury were significantly lower (by severity of the primary insult. Studies in our laboratory have 60%) than in the corresponding normal animals. Moreover, the shown that injured CNS neurons can benefit from active or rate of retinal ganglion cell survival was higher when the optic passive immunization with CNS myelin-associated antigens. nerve injury was preceded by an unrelated CNS (spinal cord) The fact that autoimmune T-cells can be both beneficial and injury in the resistant strains but not in the susceptible strains. destructive, taken together with the established phenomenon It thus seems that, in normal animals of EAE-resistant strains of genetic predisposition to autoimmune diseases, raises the (but not of susceptible strains), the injury evokes an endoge- question: will genetic predisposition to autoimmune diseases nous protective response that is T-cell dependent. These find- affect the outcome of traumatic insult to the CNS? Here we ings imply that a protective T-cell-dependent response and show that the survival rate of retinal ganglion cells in adult mice resistance to autoimmune disease are regulated by a common or rats after crush injury of the optic nerve or intravitreal injec- mechanism.
    [Show full text]
  • Neuroinflammation New Insights Into Beneficial and Detrimental Functions
    Neuroinflammation New Insights into Beneficial and Detrimental Functions Neuroinflammation New Insights into Beneficial and Detrimental Functions Edited by SAMUEL DAVID, PhD Copyright © 2015 by Wiley-Blackwell. All rights reserved Published by John Wiley & Sons, Inc., Hoboken, New Jersey Published simultaneously in Canada No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, (978) 750-8400, fax (978) 750-4470, or on the web at www.copyright.com. Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, (201) 748-6011, fax (201) 748-6008, or online at http://www.wiley.com/go/permission. Limit of Liability/Disclaimer of Warranty: While the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose.No warranty may be created or extended by sales representatives or written sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional where appropriate. Neither the publisher nor author shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
    [Show full text]
  • How Do Immune Cells Support and Shape the Brain in Health, Disease, and Aging?
    The Journal of Neuroscience, November 6, 2013 • 33(45):17587–17596 • 17587 Symposium How Do Immune Cells Support and Shape the Brain in Health, Disease, and Aging? Michal Schwartz,1 Jonathan Kipnis,2 Serge Rivest,3 and Alexandre Prat4 1Department of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel, 2Center for Brain Immunology and Glia, Department of Neuroscience, University of Virginia, Charlottesville, Virginia 22908, 3Neuroscience Laboratory, CHU de Que´bec Research Center and Department of Molecular Medicine, Faculty of Medicine, Laval University, Quebec City, Quebec G1V 4G2, Canada, and 4Neuroimmunology Unit, Center for Excellence in Neuromics, CRCHUM, Universite´ de Montre´al, Montreal, Quebec H4A 2B4, Canada For decades, several axioms have prevailed with respect to the relationships between the CNS and circulating immune cells. Specifically, immune cell entry was largely considered to be pathological or to mark the beginning of pathology within the brain. Moreover, local inflammation associated with neurodegenerative diseases such Alzheimer’s disease or amyotrophic lateral sclerosis, were considered similar in their etiology to inflammatory diseases, such as remitting relapsing-multiple sclerosis. The ensuing confusion reflected a lack of awareness that the etiology of the disease as well as the origin of the immune cells determines the nature of the inflammatory response, and that inflammation resolution is an active cellular process. The last two decades have seen a revolution in these prevailing dogmas, with a significant contribution made by the authors. Microglia and infiltrating monocyte-derived macrophages are now known to be functionally distinct and of separate origin. Innate and adaptive immune cells are now known to have protective/healing properties in the CNS, as long as their activity is regulated, and their recruitment is well controlled; their role is appreciated in maintenance of brain plasticity in health, aging, and chronic neurodevelopmental and neurodegenerative diseases.
    [Show full text]
  • Optimisé Pour L'impression
    Original article Potential immunotherapy for Alzheimer disease and age-related dementia Michal Schwartz, PhD; Michal Arad, PhD; Hila Ben-Yehuda, PhD Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain’s pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain’s disease hallmarks. Here, we provide a short review of the mechanisms orches - trating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD. © 2019, AICH – Servier Group Dialogues Clin Neurosci. 2019;21:21-25 Keywords: Alzheimer disease; immune checkpoint; immunotherapy; macrophage; microglia Introduction inflammatory drugs to arrest the brain inflammation. Inconsistent and even conflicting results were obtained, Alzheimer disease (AD) is a devastating age-related neu- and none of the drugs tested thus far have proven effec- rodegenerative disorder, and the most frequent cause of tive in reversing or arresting cognitive loss in patients.10-16 senile dementia.1 The appearance of cognitive decline is associated with accumulation of misfolded proteins, as The failure of treatments directed at Aβ to arrest or well
    [Show full text]
  • DAY 1 Monday | September 26, 2016
    SCIENTIFIC PROGRAM DAY 1 Monday | September 26, 2016 MORNING SESSION 09.15 – 13.00 ROOM A: USSISHKIN Chairs: Gianvito Martino, Hugh Willison and V. Wee Yong 09.15 INTRODUCTION TO THE COURSE Gianvito Martino, Hugh Willison and V. Wee Yong 09.30 MICROGLIA IN DEVELOPMENT AND DISEASE Luca Muzio, San Raffaele Hospital (Milan, Italy) 10.15 OLIGODENDROCYTES IN NEUROIMMUNOLOGICAL DISORDERS Jack Antel, McGill University (Montreal, Canada) 11.00 Coffee Break 11.30 ASTROCYTES AS KEY REGULATORS OF NEUROINFLAMMATION Francisco Quintana, Brigham and Women’s Hospital, Harvard Medical School (Boston, MA, USA) 12.15 NEURONS IN CNS INFLAMMATORY DISORDERS Frauke Zipp, University Medical Center of the Johannes Gutenberg University (Mainz, Germany) LUNCH BREAK 13.00 – 14.30 POSTER HALL: AGAM FOYER AFTERNOON SESSION 14.30 – 18.00 ROOM A: USSISHKIN Chairs: Gianvito Martino, Hugh Willison and V. Wee Yong 14.30 MITOCHONDRIA AND NEUROPROTECTION Don Mahad, University of Edinburg (Edinburgh, UK) 15.15 BRAIN AGING AND NEURODEGENERATION Tony Wyss-Coray, Stanford School of Medicine (Stanford, CA, USA) 1 Vers. 6 16.00 Coffee break 16.30 FUNDAMENTALS OF PSYCHONEUROIMMUNOLOGY: IMPLICATIONS IN NEUROIMMUNOLOGICAL DISORDERS Asya Rolls, Rappaport Institute of Medical Research, Technion (Haifa, Israel) 17.15 VIRUSES IN NEUROIMMUNOLOGICAL DISORDERS Yoshihisa Yamano, St. Marianna University School of Medicine (Kawasaki, Japan) 2 Vers. 6 DAY 2 Tuesday | September 27, 2016 WELCOME ADDRESS 08.00 – 08.30 ROOM A: USSISHKIN Minister of Health Michal Schwartz V. Wee Yong Dimitrios Karussis
    [Show full text]
  • A Conceptual Revolution in the Relationships Between the Brain And
    Brain, Behavior, and Immunity 25 (2011) 817–819 Contents lists available at ScienceDirect Brain, Behavior, and Immunity journal homepage: www.elsevier.com/locate/ybrbi Brief Commentary A conceptual revolution in the relationships between the brain and immunity ⇑ Michal Schwartz a,1, Jonathan Kipnis b, a The Department of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel b Department of Neuroscience, University of Virginia, Charlottesville, VA 22908, USA The perception of brain–immune interactions has dramatically We introduced and named this concept, ‘‘protective autoimmu- changed over the past decade. Current neuroimmunology has nity’’, proposing that T cells recognizing self-antigens defend moved from classic studies focusing on how immune cells can against internal threats, in analogy to T cells recognizing non-self damage the brain into a field acknowledging that the immune sys- antigens that fight external threats (Moalem et al., 1999; Schwartz tem plays a key role in maintaining the brain and in supporting its and Kipnis, 2002). (b) Infiltrating blood-derived macrophages in plasticity. Such a redefinition of this field is manifested by studies the form of ‘alternatively-activated’ macrophages (M-2 and mye- focused on understanding how innate and adaptive immune re- loid-derived suppressor cells) are locally required to heal the trau- sponses contribute to the brain’s functionality, and how to boost matized or diseased brain (Derecki et al., 2011; Rapalino et al., or modify these activities, rather than fully suppressing them, in 1998; Shechter et al., 2009). (c) Most acute and chronic neurode- the treatment of multiple pathologies including Alzheimer’s dis- generative diseases include a local inflammatory component, ease, Parkinson’s disease, multiple sclerosis, age-related dementia, though systemic anti-inflammatory compounds fail to arrest neur- mental dysfunction and other neurological diseases in which local oinflammation (Schwartz and Shechter, 2010b).
    [Show full text]