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.
References
Cotter R, Williams C, Ryan L, Lopez A, Peng H, Zheng J (2002). Fractalkine and brain inflammation: implications for HIV-1 associated dementia. J NeuroVirol 8: 585–598.
Cho C, Miller RJ (2002). Chemokine receptors and neural function. J NeuroVirol 8: 573–584.
Chowdhury IH, Bentsman G, Choe W, Potash MJ, Volsky DJ (2002). The macrophage response to HIV-1: intracellular control of X4 virus replication accompanied by activation of chemokine and cytokine synthesis. J NeuroVirol 8: 599–610.
Dinkel K, Ogle WO, Sapolsky RM (2002). Glucocorticoids and CNS inflammation. J NeuroVirol 8: 513–528.
Gendelman HE, Folks DG (1999). Innate and acquired immunity in neurodegenerative disorders. J Leuk Biol 65: 407–408.
Gendelman HE, Rappaport J, Hickey W (1999). The blood-brain barrier: a defensive shield or a perpetrator of microbial invasion. J NeuroVirol 6: 533–537.
Havilioglu N, Yuan L, Tang H, Wu JY (2002). Slit proteins, potential endogenous modoulators of inflammation. J NeuroVirol 8: 486–495.
Langford D, Masliah E (2002). Role of trophic factors on neuroimmunity in neurodegenerative infectious diseases. J NeuroVirol 8: 625–638.
Mattson MP (2002). Oxidative stress, perturbed calcium homeostasis, and immune dysfunction in Alzheimer’s disease. J NeuroVirol 8: 539–550.
McGeer PL, McGeer EG (2002). Local neuroinflammation and the progression of Alzheimer’s disease. J NeuroVirol 8: 529–538.
O’Keefe GM, Benveniste T (2002). Regulation and function of class II MHC. J NeuroVirol 8: 496–512.
Perry SW, Dewhurst S, Bellizzi MJ, Gelbard HA (2002). Conflicting effects of TNF-α in normal and diseased brain: intraneuronal receptor crosstalk as one mechanism for explaining the paradox. J NeuroVirol 8: 611–624.
Ragozzino D (2002). CXC chemokine receptors in the CNS. J NeuroVirol 8: 559–572.
Schwartz M (2002). Autoimmunity as the body’s defense mechanism against the enemy within. J NeuroVirol 8: 480–485.
Wu DC, Tieu K, Cohen O, Dong-Kug C, Vila M, Jackson-Lewis V, Teismann T, Przedborski S (2002). Glial cell response: a pathogenic factor in Parkinson’s disease. J NeuroVirol 8: 551–558.
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The research activities were supported in part by National Institutes of Health grants 2R37 NS 3613, PO1 NS 31492, 2R01 NS3423, and P01 MH050244.
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Gendelman, H.E. Neural immunity: Friend or foe?. Journal of NeuroVirology 8, 474–479 (2002). https://doi.org/10.1080/13550280290168631
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DOI: https://doi.org/10.1080/13550280290168631