Multiple sclerosis

Hafler, David A.

doi:10.1172/jci21357

Cited by 315 publications

(125 citation statements)

References 95 publications

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“…The disease often begins in young adulthood with recurrent inflammatory attacks against the white matter of the brain, involving neurological impairment, e.g. blindness, loss of sensation, lack of coordination, bowel and bladder incontinence, and difficulty in walking [47][48][49].…”

Section: Equivocal Roles Of the Nervous System And The Immune System mentioning

confidence: 99%

“…The pathological/histological hallmark of MS is the plaque, which is an area of myelin that has been damaged by inflammation and by non-neural CNS cells, including bone marrow-derived microglia and brain-derived astroglia cells [47][48][49]. The originating cause of MS is uncertain [47][48][49].…”

Section: Equivocal Roles Of the Nervous System And The Immune System mentioning

confidence: 99%

“…The originating cause of MS is uncertain [47][48][49]. Both the wound itself and the process of its repair evoke a cascade of immunological activities.…”

Section: Equivocal Roles Of the Nervous System And The Immune System mentioning

confidence: 99%

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Janus head: the dual role of HLA-G in CNS immunity

Huang¹,

Airas

Schwab³

et al. 2010

Cell. Mol. Life Sci.

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The central nervous system (CNS) is considered an immune-privileged organ that maintains an adaptable immune surveillance system. Dysregulated immune function within the CNS contributes to the development of brain tumor growth, and robust immune activation results in excessive inflammation. Human lymphocyte antigen-G (HLA-G) proteins with tolerogenic immunoreactivity have been implicated in various pathophysiological processes including immune surveillance, governing homeostasis and immune regulation. In this review, we describe the wealth of evidence for the involvement of HLA-G in the CNS under physiological and pathological conditions. Further, we review regulatory functions that may be applicable as beneficial strategies in the therapeutic manipulation of immune-mediated CNS immune responses. Additionally, we try to understand how this molecule cooperates with other CNS-resident cells to maintain normal immune homeostasis, while still facilitating the development of the appropriate immune responses.

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Section: Equivocal Roles Of the Nervous System And The Immune System mentioning

confidence: 99%

Section: Equivocal Roles Of the Nervous System And The Immune System mentioning

confidence: 99%

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Janus head: the dual role of HLA-G in CNS immunity

Huang¹,

Airas

Schwab³

et al. 2010

Cell. Mol. Life Sci.

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“…It is the leading cause of neurological disability in young adults and middle-aged people in the developed world [1], affecting 0.05-0.15% of patients of Caucasian ancestry. MS is considered to be a T-cell-mediated autoimmune disease, with pathogenic T cells being directed against antigens expressed in the CNS [2,3,4]. Immune cell infiltration of the brain and spinal cord and the subsequent plaque formation are the key characteristics of MS [4,5].…”

Section: Introductionmentioning

confidence: 99%

Cell-Based Modulation of Autoimmune Responses in Multiple Sclerosis and Experimental Autoimmmune Encephalomyelitis: Therapeutic Implications

Mastorodemos

Ιωάννου

Verginis

2014

Neuroimmunomodulation

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Multiple sclerosis (MS) is a prototypic autoimmune inflammatory disorder of the central nervous system (CNS). MS pathogenesis is a complex phenomenon that is influenced by genetic and environmental factors that lead to the dysregulation of immune homeostasis and tolerance. It has been shown that pathogenic T lymphocyte subsets, such as T helper 1 (Th1) and Th17 cells, play a crucial role in the autoimmune cascade influencing disease initiation, progression and subsequent tissue damage during MS. On the other hand, several mechanisms have been described in both patients and animal models of MS with the potential to modulate myelin-specific autoimmune responses and to facilitate amelioration of disease pathology. To this end, regulatory T cells (Tregs) are considered to be a powerful cell subset not only in the maintenance of homeostasis but also in the re-establishment of tolerance. Along these lines, other cell subsets such as dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), γδ T cells and natural killer (NK) cells have been shown to regulate the autoimmune response in the CNS under certain circumstances. This review will attempt to summarize the relevant knowledge of the regulatory mechanisms exerted by immune cells in MS that could hold the promise for the design of novel therapeutic strategies.

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“…It is believed to occur in individuals with genetic susceptibility. [173][174][175][176] Disease in these individuals might be initiated by an environmental stimulus, which results in an inflammatory response directed towards CNS targets. The resulting autoimmune response leads to demyelination and axonal degeneration within the CNS.…”

Section: Aim 2 Introductionmentioning

confidence: 99%

Antibodies to Heterogenous Nuclear Ribonucleoprotein A1 Penetrate Neurons Leading to Multiple Downstream Effects Resulting in Neurodegeneration

Douglas¹

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Multiple sclerosis

Cited by 315 publications

References 95 publications

Janus head: the dual role of HLA-G in CNS immunity

Janus head: the dual role of HLA-G in CNS immunity

Cell-Based Modulation of Autoimmune Responses in Multiple Sclerosis and Experimental Autoimmmune Encephalomyelitis: Therapeutic Implications

Antibodies to Heterogenous Nuclear Ribonucleoprotein A1 Penetrate Neurons Leading to Multiple Downstream Effects Resulting in Neurodegeneration

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