Protective effects of microglia in multiple sclerosis

Napoli, Isabella; Neumann, Harald

doi:10.1016/j.expneurol.2009.04.024

Cited by 151 publications

(123 citation statements)

References 49 publications

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“…When microglial accumulation was inhibited by 3 mM ATP or a NOS inhibitor, there was a significant reduction in total sprout lengths compared with controls when microglial accumulation was reduced (640). Thus, in the leech nervous system, microglial cells are important elements to control regeneration (631).…”

Section: Evolutionary Origins Of Microgliamentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,138

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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Section: Evolutionary Origins Of Microgliamentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,138

2,981

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“…Autoreactive T cells activate in the periphery, cross the blood-brain barrier to enter the central nervous system (CNS) and serve as important disease initiators, affecting both the local cytokine milieu and the recruitment and activation of various effector cells (7)(8)(9). Microglia and macrophages also contribute to EAE; they produce cytokines that promote inflammation during induction, but also phagocytose and clear apoptotic cell bodies, debris and inhibitory substances that limit remyelination and axon regeneration (10,11). The molecular mechanisms that control expansion, activation and CNS trafficking of myelin-specific autoreactive T cells and the complex functions of microglia and macrophages in EAE are incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion

Chinnasamy

Lutz

Riascos-Bernal

et al. 2015

Mol Med

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“…Microglia represent a likely candidate for mounting an immune response to demyelination of trigeminal afferents. In multiple sclerosis, or the animal model autoimmune encephalomyelitis, microglia respond to a lesion by phagocytosing damaged tissue and promoting neural regeneration [54]. Ironically, it is perhaps these mechanisms that are detrimental in the case of nociceptive primary afferent neurons [55].…”

Section: Trigeminal Neuralgiamentioning

confidence: 99%

Painful Neuron-Microglia Interactions in the Trigeminal Sensory System

Davies¹,

Kim²,

Oh³

2010

TOPAINJ

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Abstract:The trigeminal sensory system is unique in its innervation of structures specific to the orofacial area. Nociceptive trigeminal afferents are known to synapse with second-order neurons in the trigeminal subnucleus caudalis (Sp5C) in the brain stem. The activity of neurons within the Sp5C is responsible for the relay of nociceptive signals to higher brain centers. Recent evidence suggests that central sensitization may be fundamental to many trigeminal-specific painful neuropathies, including trigeminal neuralgia and migraine.Glia within the Sp5C are emerging as prime suspects in trigeminal central sensitization. In particular, microglial activation has been implicated in the development of neuropathic pain. It is possible that activated microglia release factors that alter the activity of second-order neurons or the synaptic activity of peripheral terminals within the Sp5C.Microglial activation has been characterized by changes in morphology, expression of membrane receptors and ion channels, as well as alterations to cytokine and chemokine release. In addition, microglia have been studied in brain slice and dissociated culture where activation is characterized by changes to P2X receptor and potassium channel membrane currents. However, little is known about resting and activated microglial membrane properties in the Sp5C and, furthermore, how these properties are affected following trigeminal nerve injury. This review summarizes the anatomical and pathophysiological importance of the Sp5C and focuses on recent studies on neurons and microglia in the trigeminal sensory system. The final part of the review aims to link important aspects of microglial membrane physiology with their potential role in chronic trigeminal pain conditions.

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Protective effects of microglia in multiple sclerosis

Cited by 151 publications

References 49 publications

Physiology of Microglia

Physiology of Microglia

Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion

Painful Neuron-Microglia Interactions in the Trigeminal Sensory System

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