Viral Inhibitors and Immune Response Mediators: The Interferons

Meager, Anthony

doi:10.1002/3527600906.mcb.200500008

Cited by 6 publications

(5 citation statements)

References 59 publications

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“…The main function of cytokines is the regulation of T-cell differentiation from undifferentiated cells to T-helper 1 and 2, regulatory T cells, and T-helper 17 cells [ 101 ]. These regulatory proteins include ILs, interferons (IFNs), colony stimulating factors (CSFs), TNFs, and certain growth factors (GFs) [ 102 , 103 ].…”

Section: Inflammatory Process In Alzheimer's Diseasementioning

confidence: 99%

A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines

Rubio-Pérez

Morillas-Ruiz

2012

The Scientific World Journal

674

495

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Alzheimer's disease (AD) is the most common neurodegenerative disorder to date. Neuropathological hallmarks areβ-amyloid (Aβ) plaques and neurofibrillary tangles, but the inflammatory process has a fundamental role in the pathogenesis of AD. Inflammatory components related to AD neuroinflammation include brain cells such as microglia and astrocytes, the complement system, as well as cytokines and chemokines. Cytokines play a key role in inflammatory and anti-inflammatory processes in AD. An important factor in the onset of inflammatory process is the overexpression of interleukin (IL)-1, which produces many reactions in a vicious circle that cause dysfunction and neuronal death. Other important cytokines in neuroinflammation are IL-6 and tumor necrosis factor (TNF)-α. By contrast, other cytokines such as IL-1 receptor antagonist (IL-1ra), IL-4, IL-10, and transforming growth factor (TGF)-βcan suppress both proinflammatory cytokine production and their action, subsequently protecting the brain. It has been observed in epidemiological studies that treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) decreases the risk for developing AD. Unfortunately, clinical trials of NSAIDs in AD patients have not been very fruitful. Proinflammatory responses may be countered through polyphenols. Supplementation of these natural compounds may provide a new therapeutic line of approach to this brain disorder.

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Section: Inflammatory Process In Alzheimer's Diseasementioning

confidence: 99%

A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines

Rubio-Pérez

Morillas-Ruiz

2012

The Scientific World Journal

674

495

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“…In the same manner, changes in levels of many cytokines have been described not only in AD brains but also in blood and cerebrospinal fluid from patients. Thus, increased levels of IL-1 α , IL-1 β , IL-6, TNF- α , and GM-SF have been reported in brain tissue [71, 72]. In serum from patients, an increase in eotaxin, a cytokine recently linked to adult neurogenesis and ageing has been also detected [28] and, correlating to this, an increase in the expression of its receptor, CCR3, has been found in AD brains, especially in microglia [73].…”

Section: Neuroinflammation and Alzheimer Diseasementioning

confidence: 99%

Role of Neuroinflammation in Adult Neurogenesis and Alzheimer Disease: Therapeutic Approaches

Fuster-Matanzo

Llorens‐Martin

Hernández

et al. 2013

Mediators of Inflammation

127

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Neuroinflammation, a specialized immune response that takes place in the central nervous system, has been linked to neurodegenerative diseases, and specially, it has been considered as a hallmark of Alzheimer disease, the most common cause of dementia in the elderly nowadays. Furthermore, neuroinflammation has been demonstrated to affect important processes in the brain, such as the formation of new neurons, commonly known as adult neurogenesis. For this, many therapeutic approaches have been developed in order to avoid or mitigate the deleterious effects caused by the chronic activation of the immune response. Considering this, in this paper we revise the relationships between neuroinflammation, Alzheimer disease, and adult neurogenesis, as well as the current therapeutic approaches that have been developed in the field.

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“…Brain inflammation is one of the most important risk factors for sporadic AD development (Guerreiro et al, 2013). Aβ peptides and APP activate glial cells (Barger and Harmon, 1997;Dickson et al, 1993), leading to cytokine and chemokine production (including Interleukin 1 (IL1 ) and Interferon gamma (IFNγ)) and, therefore, to increased cytokine and chemokine expression in the AD brain (Meager 2004;2005;Ho et al, 2005). Cytokines can also induce Aβ generation, tau phosphorylation and oxidative stress (Steel et al, 2007;Blurton-Jones and Laferla, 2006;Sastre et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Anti-IL17 treatment ameliorates Down syndrome phenotypes in mice

Rueda

Vidal

García-Cerro

et al. 2018

Brain, Behavior, and Immunity

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Down syndrome (DS) is characterized by structural and functional anomalies that are present prenatally and that lead to intellectual disabilities. Later in life, the cognitive abilities of DS individuals progressively deteriorate due to the development of Alzheimer's disease (AD)-associated neuropathology (i.e., β-amyloid (Aβ) plaques, neurofibrillary tangles (NFTs), neurodegeneration, synaptic pathology, neuroinflammation and increased oxidative stress). Increasing evidence has shown that among these pathological processes, neuroinflammation plays a predominant role in AD etiopathology. In AD mouse models, increased neuroinflammation appears earlier than Aβ plaques and NFTs, and in DS and AD models, neuroinflammation exacerbates the levels of soluble and insoluble Aβ species, favoring neurodegeneration. The Ts65Dn (TS) mouse, the most commonly used murine model of DS, recapitulates many alterations present in both DS and AD individuals, including enhanced neuroinflammation. In this study, we observed an altered neuroinflammatory milieu in the hippocampus of the TS mouse model. Pro-inflammatory mediators that were elevated in the hippocampus of this model included pro-inflammatory cytokine IL17A, which has a fundamental role in mediating brain damage in neuroinflammatory processes. Here, we analyzed the ability of an anti-IL17A antibody to reduce the neuropathological alterations that are present in TS mice during early neurodevelopmental stages (i.e., hippocampal neurogenesis and hypocellularity) or that are aggravated in later-life stages (i.e., cognitive abilities, cholinergic neuronal loss and increased cellular senescence, APP expression, Aβ peptide expression and neuroinflammation). Administration of anti-IL17 for 5 months, starting at the age of 7 months, partially improved the cognitive abilities of the TS mice, reduced the expression of several pro-inflammatory cytokines and the density of activated microglia and normalized the APP and Aβ levels in the hippocampi of the TS mice. These results suggest that IL17-mediated neuroinflammation is involved in several AD phenotypes in TS mice and provide a new therapeutic target to reduce these pathological characteristics.

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Viral Inhibitors and Immune Response Mediators: The Interferons

Cited by 6 publications

References 59 publications

A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines

A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines

Role of Neuroinflammation in Adult Neurogenesis and Alzheimer Disease: Therapeutic Approaches

Anti-IL17 treatment ameliorates Down syndrome phenotypes in mice

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