Journal of NeuroVirology

, Volume 8, Issue 6, pp 474–479 | Cite as

Neural immunity: Friend or foe?

  • Howard E. Gendelman
Guest Editorial


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.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 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.CrossRefPubMedGoogle Scholar
  2. Cho C, Miller RJ (2002). Chemokine receptors and neural function. J NeuroVirol 8: 573–584.CrossRefPubMedGoogle Scholar
  3. 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.CrossRefPubMedGoogle Scholar
  4. Dinkel K, Ogle WO, Sapolsky RM (2002). Glucocorticoids and CNS inflammation. J NeuroVirol 8: 513–528.CrossRefPubMedGoogle Scholar
  5. Gendelman HE, Folks DG (1999). Innate and acquired immunity in neurodegenerative disorders. J Leuk Biol 65: 407–408.Google Scholar
  6. 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.CrossRefGoogle Scholar
  7. Havilioglu N, Yuan L, Tang H, Wu JY (2002). Slit proteins, potential endogenous modoulators of inflammation. J NeuroVirol 8: 486–495.CrossRefGoogle Scholar
  8. Langford D, Masliah E (2002). Role of trophic factors on neuroimmunity in neurodegenerative infectious diseases. J NeuroVirol 8: 625–638.CrossRefPubMedGoogle Scholar
  9. Mattson MP (2002). Oxidative stress, perturbed calcium homeostasis, and immune dysfunction in Alzheimer’s disease. J NeuroVirol 8: 539–550.CrossRefPubMedGoogle Scholar
  10. McGeer PL, McGeer EG (2002). Local neuroinflammation and the progression of Alzheimer’s disease. J NeuroVirol 8: 529–538.CrossRefPubMedGoogle Scholar
  11. O’Keefe GM, Benveniste T (2002). Regulation and function of class II MHC. J NeuroVirol 8: 496–512.CrossRefPubMedGoogle Scholar
  12. 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.CrossRefPubMedGoogle Scholar
  13. Ragozzino D (2002). CXC chemokine receptors in the CNS. J NeuroVirol 8: 559–572.CrossRefPubMedGoogle Scholar
  14. Schwartz M (2002). Autoimmunity as the body’s defense mechanism against the enemy within. J NeuroVirol 8: 480–485.CrossRefPubMedGoogle Scholar
  15. 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.CrossRefPubMedGoogle Scholar

Copyright information

© Journal of NeuroVirology, Inc. 2002

Authors and Affiliations

  1. 1.The Center for Neurovirology and Neurodegenerative Disorders, The Departments of Pathology and Microbiology, Internal Medicine and PsychiatryUniversity of Nebraska Medical CenterOmahaUSA

Personalised recommendations