Role of the innate immune system in the pathogenesis of multiple sclerosis

Gandhi, Roopali; Laroni, Alice; Weiner, Howard L.

doi:10.1016/j.jneuroim.2009.10.015

Cited by 281 publications

(213 citation statements)

References 148 publications

(164 reference statements)

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“…Further research divided these NK cells into even smaller subsets, recognized as NK22 secreting IL-22 and found in lymphoid tissues of the gastrointestinal tract [94] , or NK17/NK1 cells secreting IL-17 and IFN-γ when stimulated with IL-2 [95] . The role of NK cells in autoimmune diseases is being investigated, and is highly debated as both positive and negative associations have been observed [96][97][98][99] . In the EAE model, depletion of NK cells resulted in a severe relapsing EAE, and more pronounced CNS pathology [100][101][102][103] .…”

Section: Cd56mentioning

confidence: 99%

Multiple sclerosis and the role of immune cells

Høglund

Maghazachi

2014

WJEM

135

101

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Multiple sclerosis (MS) is a complex disease with many different immune cells involved in its pathogenesis, and in particular T cells as the most recognized cell type. Recently, the innate immune system has also been researched for its effect on the disease. Hence, cells of the immune system play vital roles in either ameliorating or exacerbating the disease. The genetic and environmental factors, as well as the etiology and pathogenesis are of utmost importance for the development of MS. An insight into the roles play by T cells, B cells, natural killer cells, and dendritic cells in MS and the animal model experimental autoimmune encephalomyelitis, will be presented. Understanding the mechanisms of action for current therapeutic modalities should help developing new therapeutic tools to treat this disease and other autoimmune diseases.

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Section: Cd56mentioning

confidence: 99%

Multiple sclerosis and the role of immune cells

Høglund

Maghazachi

2014

WJEM

135

101

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“…Although the precise trigger for MS remains elusive, resident microglia and blood-derived monocytes or macrophages seem to play a central role in the pathogenesis of MS and EAE (for review, see Gandhi et al 2010;Almolda et al 2011;Chastain et al 2011). Elimination of macrophages or microglia suppresses clinical and histopathological manifestations in rodent models of MS (Brosnan et al 1981;Huitinga et al 1990;Bauer et al 1995;Polfliet et al 2002;Heppner et al 2005), and infiltrating blood-borne monocytes trigger EAE progression to the severe form of the disease (Ajami et al 2011).…”

mentioning

confidence: 99%

Upregulation of Vascular Endothelial Growth Factor Receptor-3 in the Spinal Cord of Lewis Rats with Experimental Autoimmune Encephalomyelitis

Park

Shin

Cho

et al. 2012

J Histochem Cytochem.

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We investigated the spatiotemporal expression of vascular endothelial growth factor receptor–3 (VEGFR-3) in the spinal cord of Lewis rats with experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. VEGFR-3 mRNA and protein were constitutively expressed in gray matter neurons and in a few white matter astrocytes. Induction of VEGFR-3 occurred predominantly in perivascular infiltrated macrophages in the spinal cord white matter during the inductive phase of EAE. VEGFR-3 expression was also induced in activated microglial cells in the gray and white matter, mainly in the peak phase. In addition, reactive astrocytes in the white matter, but not in the gray matter, expressed VEGFR-3 as disease severity increased. These data suggest that VEGFR-3 is involved in the recruitment of monocytic macrophages and in glial reactions during EAE.

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“…Impairment of NK cell cytotoxicity has been implicated in autoimmune disease 49 . NK cell cytotoxicity and pro-inflammatory activities may at first seem deleterious, but the human CD56 bright subset, best known for secreting pro-inflammatory factors rather than NK cytotoxic activity, is associated with responses to biologics in multiple sclerosis (MS), and murine NK cells, at least, can secrete restorative neurotropic factors such as brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3) 50 . In Lyme arthritis, there appear to be elevated levels of activated IFN-γ-producing CD56 bright NK cells in synovial fluid, whether antibiotic resistant or not, suggesting that these cells contribute to excessive inflammation and immune dysregulation in joints 55 .…”

Section: Nk Cells In Autoimmunitymentioning

confidence: 99%