Is Central Nervous System an Immune-Privileged Site?

Shrestha, Robin; Millington, Owain R.; Brewer, James M.; Bushell, Trevor J.

doi:10.3126/kumj.v11i1.11055

Cited by 21 publications

(9 citation statements)

References 91 publications

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“…136,138 The classical view that regarded the CNS as an immune-privileged site by virtue of the imperm eable blood-brain barrier has evolved to a view of significant interactions between the CNS and immune system. 139 Through such processes, cells of the nervous system such as microglia, astrocytes, oligodendrocytes, Schwann cells in the peripheral nervous system, endothelial cells of the brain microvasculature, and even neurons can release cytokines and chemokines (Figure 3). 139 Finally, notable changes in neurotransmitter levels have been detected in male Wistar rat models of AKI, including decreased dopamine turnover in the striatum, mesencephalon, and hypothalamus, which can substantially effect learning, memory, anxiety, and depression.…”

Section: Cognitive Impairment In Uraemiamentioning

confidence: 99%

Kidney–brain crosstalk in the acute and chronic setting

et al. 2015

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Patients with kidney disease often exhibit multiple organ dysfunction that is caused, in part, by marked connectivity between the kidney and other organs and tissues. Substantial crosstalk occurs between the kidney and the brain, as indicated by the frequent presentation of neurological disorders, such as cerebrovascular disease, cognitive impairment, and neuropathy during the natural history of chronic kidney disease. The underlying pathophysiology of such comorbid neurological disorders in kidney disease is governed by shared anatomic and vasoregulatory systems and humoral and non-humoral bidirectional pathways that affect both the kidney and the brain. During acute kidney injury, the brain and kidney might interact through the amplification of cytokine-induced damage, extravasation of leukocytes, oxidative stress, and dysregulation of sodium, potassium, and water channels. The advent of dialysis and renal transplantation programmes has led to a reduction in the rate of neurological complications associated with uraemia, but a new set of complications have arisen as a consequence of the effects of dialysis on the central nervous system over the short and long term. This Review discusses the clinical complications of acute and chronic renal failure from a neurologic perspective, and highlights current understanding of the underlying pathophysiologies.

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Section: Cognitive Impairment In Uraemiamentioning

confidence: 99%

Kidney–brain crosstalk in the acute and chronic setting

et al. 2015

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“…Consequently, one might conclude that the signaling effects of rituximab on B cells may contribute to the anti-tumor activity of rituximab in a manner that is not relevant to immune participation. Although, we must be cautious since more recent observations have suggested that the central nervous system is not an immune-privileged but rather it could be considered as an active surveillance site where activated immune cells can cross the blood-brain barrier (Shrestha et al, 2013).…”

Section: Chemosensitizationmentioning

confidence: 99%

A molecular perspective on rituximab: A monoclonal antibody for B cell non Hodgkin lymphoma and other affections

Seyfizadeh

Hasenkamp

Huerta-Yépez

2016

Critical Reviews in Oncology/Hematology

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“…The brain has been considered to be an “immune-privileged” organ, isolated from the peripheral immune system (Shrestha et al, 2013). However, recent evidence shows that there is bi-directional communication between the brain and the peripheral immune system (Holmes and Butchart, 2011).…”

Section: Systemic Inflammation and Admentioning

confidence: 99%

Systemic inflammation, blood-brain barrier vulnerability and cognitive/non-cognitive symptoms in Alzheimer disease: relevance to pathogenesis and therapy

Takeda

Sato

Morishita

2014

Front. Aging Neurosci.

184

112

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The incidence of dementia is increasing at an alarming rate, and has become a major public health concern. Alzheimer disease (AD) is the most common form of dementia and is characterized by progressive cognitive impairment. In addition to classical neuropathological features such as amyloid plaques and neurofibrillary tangles (NFT), accumulation of activated immune cells has been documented in the AD brain, suggesting a contribution of neuroinflammation in the pathogenesis of AD. Besides cognitive deterioration, non-cognitive symptoms, such as agitation, aggression, depression and psychosis, are often observed in demented patients, including those with AD, and these neuropsychological symptoms place a heavy burden on caregivers. These symptoms often exhibit sudden onset and tend to fluctuate over time, and in many cases, they are triggered by an infection in peripheral organs, suggesting that inflammation plays an important role in the pathogenesis of these non-cognitive symptoms. However, there is no mechanistic explanation for the relationship between inflammation and neuropsychiatric symptoms. Observations from experimental mouse models indicate that alteration of brain blood vessels, especially blood-brain barrier (BBB) dysfunction, may contribute to the relationship. The current review summarizes the results from recent studies on the relationship between inflammation and AD, while focusing on cerebrovascular alterations, which might provide an insight into the pathogenesis of cognitive/non-cognitive symptoms in AD patients and suggest a basis for the development of new therapeutic treatments for these conditions.

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Is Central Nervous System an Immune-Privileged Site?

Cited by 21 publications

References 91 publications

Kidney–brain crosstalk in the acute and chronic setting

Kidney–brain crosstalk in the acute and chronic setting

A molecular perspective on rituximab: A monoclonal antibody for B cell non Hodgkin lymphoma and other affections

Systemic inflammation, blood-brain barrier vulnerability and cognitive/non-cognitive symptoms in Alzheimer disease: relevance to pathogenesis and therapy

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