Inflammation in multiple sclerosis: the good, the bad, and the complex

Martino, Gianvito; Adorini, Luciano; Rieckmann, Peter; Hillert, Jan; Kallmann, Boris; Comı, Gıancarlo; Filippi, Massimo

doi:10.1016/s1474-4422(02)00223-5

Cited by 143 publications

(83 citation statements)

References 120 publications

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“…The apparent protective effect of CA 12 /G haplotype, which would be expected to be associated with higher IFNg expression, seems to conflict with the hypothesis that higher IFNg expression leads to an increased Th-1 cell response and consequently greater susceptibility to MS. 59 On the other hand, some effects of IFNg-related inflammation such as inhibition of the accumulation of activated T cells by limiting antigen-induced proliferation and/or by enhancing apoptosis can actually be protective in autoimmune disorders as recently discussed by O'Shea and Paul 60 and Martino et al 61 Recent evidence by Pelfrey et al 26 and Nguyen et al 27 suggests that there is stronger Th-1/Th-2 bias in women than men with MS. The difference in frequency of the alleles between men and women may also reflect interaction between the disease, the genotype and gender, because the differences in genotype frequency are not evident in the controls.…”

Section: Discussionmentioning

confidence: 98%

IFNG polymorphisms are associated with gender differences in susceptibility to multiple sclerosis

et al. 2005

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Interferon-gamma (IFNg) treatment is deleterious in multiple sclerosis (MS). MS occurs twice as frequently in women as in men. IFNg expression varies by gender. We studied a population-based sample of US MS patients and ethnicity-matched controls and independent Northern Irish and Belgian hospital-based patients and controls for association with MS, stratified by gender, of an intron 1 microsatellite [I1 (761)

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Section: Discussionmentioning

confidence: 98%

IFNG polymorphisms are associated with gender differences in susceptibility to multiple sclerosis

et al. 2005

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“…Thus, among the putative mechanisms that trigger the activation of the autoimmune reaction, inflammation is considered pivotal and microglia are thought to play a major role by up-regulating MHC class II molecules, inflammatory cytokines, reactive oxygen and nitrogen species; on the other hand, beneficial effects of microglia activation must be taken into account, such as myelin debris fagocytosis. This led us to propose inflammation as a candidate therapeutic target for MS within selected phases of the disease [149].…”

Section: Multiple Sclerosis and Neuroinflammationmentioning

confidence: 99%

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Vegeto

Benedusi

Maggi

2008

Frontiers in Neuroendocrinology

278

206

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a b s t r a c tRecent studies highlight the prominent role played by estrogens in protecting the central nervous system (CNS) against the noxious consequences of a chronic inflammatory reaction. The neurodegenerative process of several CNS diseases, including Multiple Sclerosis, Alzheimer's and Parkinson's Diseases, is associated with the activation of microglia cells, which drive the resident inflammatory response. Chronically stimulated during neurodegeneration, microglia cells are thought to provide detrimental effects on surrounding neurons. The inhibitory activity of estrogens on neuroinflammation and specifically on microglia might thus be considered as a beneficial therapeutic opportunity for delaying the onset or progression of neurodegenerative diseases; in addition, understanding the peculiar activity of this female hormone on inflammatory signalling pathways will possibly lead to the development of selected anti-inflammatory molecules. This review summarises the evidence for the involvement of microglia in neuroinflammation and the anti-inflammatory activity played by estrogens specifically in microglia.

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“…In particular, the prevailing hypothesis is that autoreactive T cells of the CD4 + T helper (Th)1 population orchestrate the MS inflammatory pathogenetic process [2]. According to the primary inflammatory nature of this CNS disease, MS demyelinated areas are characterized by inflammatory infiltrates that contain blood-derived myelin-specific T cells, B cells, and a multitude of non-specific, effector mononuclear cells [68], and it has been demonstrated that inflammatory cytokines (such as IL1β, TNF-α) and other inflammation-related molecules (such as iNOS) are expressed in active MS plaques [68,69].…”

Section: Mitochondria: the Ultimate Target Leading To Neurodegeneratimentioning

confidence: 99%

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

Filippo

Chiasserini

Tozzi

et al. 2010

JAD

130

100

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Abstract. The innate immune response is thought to exert a dichotomous role in the brain. Indeed, although molecules of the innate immune response can promote repair mechanisms, during neuroinflammatory processes many harmful mediators are also released. Signs of neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases. Interestingly, it has been proposed that mitochondria may exert a crucial role in the pathogenesis of both inflammatory and neurodegenerative central nervous system disorders. In this review, we describe the mechanisms by which neuroinflammation and mitochondrial impairment may synergistically trigger a vicious cycle ultimately leading to neuronal death. In particular, we describe the close relationship existing among neuroinflammation, neurodegeneration, and mitochondrial impairment in three different widely-diffused neurological diseases in which these pathogenetic events coexist, namely multiple sclerosis, Parkinson's disease, and Alzheimer's disease.

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Inflammation in multiple sclerosis: the good, the bad, and the complex

Cited by 143 publications

References 120 publications

IFNG polymorphisms are associated with gender differences in susceptibility to multiple sclerosis

IFNG polymorphisms are associated with gender differences in susceptibility to multiple sclerosis

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

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