Abstract

The articles compiled in this special edition of Journal of NeuroVirology target a developing field of investigation seeking to uncover how the immune system affects both the pathogenic process and protection against the ravages of neurodegenerative processes. Whether caused by a microbe, trauma, toxic metabolite, autoimmunity, or part of a wide degenerative process, immune dysfunction commonly affects central nervous system (CNS) disease. All together, the work presented here proved to be a unique undertaking with contributing scientists outside the field of neurovirology. Indeed, multiple disciplines including molecular neuroscience, neuroimmunology, virology, cellular immunology, receptor pharmacology, neuronal electrophysiology, neurochemistry, clinical neurology, and development neurobiology were joined. The basis of this work rests with the hypothesis that brain mononuclear phagocytes (MP; perivascular and brain macrophages and microglia) act as inducers of disease by engaging the immune system to protect, defend, or induce neural injury. Indeed, it is the brain MP that act as scavengers killing microblial pathogens, regulate immune responses through antigen presentation and mobilization of adaptive immune activities, and affect the production of neurotrophic or toxic secretory factors that incite disease processes. For many years, these responses were thought to be reactive to ongoing disease mechanisms with little effects on disease itself, let alone repair. The works compiled in this issue demonstrate quite clearly this is no longer true. Immune responses cannot be directed only against a microbe but also against self-antigens that are expressed in damaged CNS, leading to innate neurotoxic or adaptive anti-self immunity that commonly follow viral infections. Importantly, therapeutic modalities may take advantage of CNS immune responses through vaccination generating neuroprotection. Together, these articles serve to bring together common neuroimmune links between highly divergent diseases (for example, Parkinson's and Alzheimer's disease and human immunodeficiency virus type-one dementia). In the end, I hope this work will serve as discussion points for future collaborations and began to break down the barriers of disease, enabling targeted research activities toward what we have in common.

Original languageEnglish (US)
Pages (from-to)474-479
Number of pages6
JournalJournal of neurovirology
Volume8
Issue number6
DOIs
StatePublished - Dec 1 2002

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Immunity
Poisons
Brain
Central Nervous System
Neurochemistry
Virology
Neurobiology
Electrophysiology
Central Nervous System Diseases
Histocompatibility Antigens Class II
Immune System Diseases
Autoantigens
Wounds and Injuries
Antigen Presentation
Microglia
Virus Diseases
Phagocytes
Neurology
Neurosciences
Allergy and Immunology

ASJC Scopus subject areas

  • Virology
  • Clinical Neurology

Cite this

Neural immunity : Friend or foe? / Gendelman, Howard Eliot.

In: Journal of neurovirology, Vol. 8, No. 6, 01.12.2002, p. 474-479.

Research output: Contribution to journalEditorial

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abstract = "The articles compiled in this special edition of Journal of NeuroVirology target a developing field of investigation seeking to uncover how the immune system affects both the pathogenic process and protection against the ravages of neurodegenerative processes. Whether caused by a microbe, trauma, toxic metabolite, autoimmunity, or part of a wide degenerative process, immune dysfunction commonly affects central nervous system (CNS) disease. All together, the work presented here proved to be a unique undertaking with contributing scientists outside the field of neurovirology. Indeed, multiple disciplines including molecular neuroscience, neuroimmunology, virology, cellular immunology, receptor pharmacology, neuronal electrophysiology, neurochemistry, clinical neurology, and development neurobiology were joined. The basis of this work rests with the hypothesis that brain mononuclear phagocytes (MP; perivascular and brain macrophages and microglia) act as inducers of disease by engaging the immune system to protect, defend, or induce neural injury. Indeed, it is the brain MP that act as scavengers killing microblial pathogens, regulate immune responses through antigen presentation and mobilization of adaptive immune activities, and affect the production of neurotrophic or toxic secretory factors that incite disease processes. For many years, these responses were thought to be reactive to ongoing disease mechanisms with little effects on disease itself, let alone repair. The works compiled in this issue demonstrate quite clearly this is no longer true. Immune responses cannot be directed only against a microbe but also against self-antigens that are expressed in damaged CNS, leading to innate neurotoxic or adaptive anti-self immunity that commonly follow viral infections. Importantly, therapeutic modalities may take advantage of CNS immune responses through vaccination generating neuroprotection. Together, these articles serve to bring together common neuroimmune links between highly divergent diseases (for example, Parkinson's and Alzheimer's disease and human immunodeficiency virus type-one dementia). In the end, I hope this work will serve as discussion points for future collaborations and began to break down the barriers of disease, enabling targeted research activities toward what we have in common.",
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