Neural immunity: Friend or foe?

  title={Neural immunity: Friend or foe?},
  author={Howard E. Gendelman},
  journal={Journal of NeuroVirology},
  • H. Gendelman
  • Published 1 December 2002
  • Biology
  • Journal of NeuroVirology
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… 

EncephalomyelitisProtects against Experimental Autoimmune Complement Factor H, a Marker of Self

It is found that the accumulation of human fH in the brain parenchyma protected neurons from complement opsonization, axonal injury, and leukocyte infiltration.

Complement Factor H, a Marker of Self Protects against Experimental Autoimmune Encephalomyelitis1

It is found that the accumulation of human fH in the brain parenchyma protected neurons from complement opsonization, axonal injury, and leukocyte infiltration, and the data argue for a key regulatory activity offH in neuroprotection and provide novel therapeutic avenues for CNS chronic inflammatory diseases.

Immune Response in Neurological Pathology: Emerging Role of Central and Peripheral Immune Crosstalk

An overview of major immune effector cells and the role of the blood-brain barrier in regard to neurological disorders is provided and targeting central-peripheral immune interactions is proposed as a potential improved therapeutic strategy to overcome failures in clinical translation.

B Cells in Multiple Sclerosis and Virus-Induced Neuroinflammation

The available literature is reviewed to explore the relationship between autoimmune and infectious neuroinflammation with a focus on the involvement of B cells in MS and viral infections of the CNS.

Neuro‐immune lessons from an annelid: The medicinal leech

Purinergic mechanisms in neuroinflammation: An update from molecules to behavior

Toxoplasma gondii: Biological Parameters of the Connection to Schizophrenia

This article provides a comprehensive review of the status of Toxoplasma research in schizophrenia, including the limitations and improvements of immune-based assays to detect these infections in humans, and recent discoveries concerning the schizophrenia-Toxoplasm association.

Immune Mechanism of Epileptogenesis and Related Therapeutic Strategies

A narrative review on the recent advances on the basic epileptogenic mechanisms related to the activation of immunity or neuroinflammation with special attention to current and future opportunities for novel treatments in epilepsy.

Persistent Toxoplasma Infection of the Brain Induced Neurodegeneration Associated with Activation of Complement and Microglia

It is suggested that chronic Toxoplasma infection leads to cortical neurodegeneration and results in CX3CL1, complement, and microglial interactions, which are known to mediate the phagocytic clearance of degenerating neurons.



Innate and acquired immunity in neurodegenerative disorders

These works uncover important but common neuroimmune links between highly divergent diseases including Alzheimer’s disease (AD), multiple sclerosis (MS), HIV-1-associated dementia (HAD), progressive multifocal leukoencephalopathy (PML), and simian immunodeficiency viral (SIV) infection of the central nervous system (CNS).

Autoimmunity as the body’s defense mechanism against the enemy within: Development of therapeutic vaccines for neurodegenerative disorders

The immune response in this case is directed against dominant self-antigens residing in the damaged site, where such an adaptive anti-self immune response reinforces the protective activity of local resident cells by providing them with factors that can augment and regulate their capacity for buffering troublemakers such as destructive self-compounds emerging from the injured neural tissue.

Role of trophic factors on neuroimmunity in neurodegenerative infectious diseases

The main objective of this review is to provide an overview of evidence in support of the role of trophic factors in regulating the neuroimmune response in chronic viral infections of the central nervous system.

The blood-brain barrier: A defensive shield or a perpetrator of microbial invasion?

A series of articles that highlight the blood-brain barrier's (BBB) importance in brain defense and microbial pathogenesis and the plethora of functions and microbes that affect BBB biology are published.

Local neuroinflammation and the progression of Alzheimer’s disease

Much epidemiological and limited clinical evidence suggests that nonsteroidal anti-inflammatory drugs may impede the onset and slow the progression of Alzheimer’s disease, but these drugs strike at the periphery of the inflammatory reaction.

Tumor necrosis factor-alpha in normal and diseased brain: Conflicting effects via intraneuronal receptor crosstalk?

Support is provided from the literature to advance the hypothesis that one mechanism by which TNF-α can exert its paradoxical effects in the brain is via crosstalk with signaling pathways of growth factors or other cytokines.

Oxidative stress, perturbed calcium homeostasis, and immune dysfunction in Alzheimer’s disease

Interestingly, immunization of AD mice with amyloid β-peptide can stimulate the immune system to remove amyloids from the brain and can ameliorate memory deficits, suggesting that it may be possible to prevent AD by bolstering immune function.

Regulation and function of class II major histocompatibility complex, CD40, and B7 expression in macrophages and microglia: Implications in neurological diseases

The molecular mechanisms underlying class II MHC, CD40 and B7 regulation in microglia and macrophages are described and their focus is on the cis-elements in the promoters of their genes and the transcription factors activated by cytokines that bind them.

Glucocorticoids and central nervous system inflammation

It is shown that under certain circumstances GCs might fail to have anti-inflammatory effects and sometimes even enhance inflammation.

Glial cell response: A pathogenic factor in Parkinson’s disease

The authors discuss the potential protective and deleterious effects of glial cells in the SNpc of PD and examine how these factors may contribute to the pathogenesis of this disease.