Absence of donor-type major histocompatibility complex class I antigen-bearing microglia in the rat central nervous system of radiation bone marrow chimeras

Matsumoto, Yoh; Fujiwara, Michio

doi:10.1016/0165-5728(87)90032-4

Cited by 111 publications

(64 citation statements)

References 19 publications

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“…Using irradiation bone marrow chimeric mice, bone marrow derived cells have been found to take up long-term residence near the site of injury in mice with facial axotomies or ischemic damage [43,44]. This response is in stark contrast to what occurs in healthy mice or in mice after EAE, or virally induced demyelinating disease [36,37,45]. In these situations, bone marrow derived cells fail to contribute to the parenchymal microglial population.…”

Section: Glial Heterogeneity: Implications For Inflammation and Neuromentioning

confidence: 99%

The cellular response in neuroinflammation: The role of leukocytes, microglia and astrocytes in neuronal death and survival

Carson

Thrash

Walter

2006

Clinical Neuroscience Research

235

156

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Neuroinflammation is a complex integration of the responses of all cells present within the CNS, including the neurons, macroglia, microglia and the infiltrating leukocytes. The initiating insult, environmental factors, genetic background and age/past experiences all combine to modulate the integrated response of this complex neuroinflammatory circuit. Here, we explore how these factors interact to lead to either neuroprotective versus neurotoxic inflammatory responses. We specifically focus on microglia and astrocytic regulation of autoreactive T cell responses.

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Section: Glial Heterogeneity: Implications For Inflammation and Neuromentioning

confidence: 99%

The cellular response in neuroinflammation: The role of leukocytes, microglia and astrocytes in neuronal death and survival

Carson

Thrash

Walter

2006

Clinical Neuroscience Research

235

156

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“…The hypothesis that microglial cells are of hemopoietic origin has been tested in mammals using bone marrow chimeras (Matsumoto and Fujiwara, 1987;Hickey and Kimura, 1988;De Groot et al, 1992;Hickey et al, 1992;Unger et al, 1993;Krall et al, 1994). One of these studies (Matsumoto and Fujiwara, 1987) failed to observe microglial cells of bone marrow origin, and concluded that microglia were probably of neuroectodermal origin.…”

Section: Origin From Primitive Hemopoietic Cellsmentioning

confidence: 99%

“…One of these studies (Matsumoto and Fujiwara, 1987) failed to observe microglial cells of bone marrow origin, and concluded that microglia were probably of neuroectodermal origin. Hickey and Kimura (1988) showed that the perivascular microglia are bone marrow-derived.…”

Section: Origin From Primitive Hemopoietic Cellsmentioning

confidence: 99%

“…In several of these studies antibodies against speci®c major histocompatibility class I antigens (MHC I) molecules were used to detect cells of donor origin (Matsumoto and Fujiwara, 1987;Hickey and Kimura, 1988;Hickey et al, 1992). Because MHC I are not constitutively expressed in normal rat brains (Flaris et al, 1993), it was necessary to induce upregulation of these molecules to disclose the presence of labeled cells.…”

Section: Origin From Primitive Hemopoietic Cellsmentioning

confidence: 99%

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The origin and differentiation of microglial cells during development

Cuadros

Navascués

1998

Progress in Neurobiology

269

177

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AbstractÐSome authors claim that microglia originate from the neuroepithelium, although most now believe that microglial cells are of mesodermal origin, and probably belong to the monocyte/macrophage cell line. These cells must enter the developing central nervous system (CNS) from the blood stream, the ventricular space or the meninges. Afterward microglial cells are distributed more or less homogeneously through the entire nervous parenchyma. Stereotyped patterns of migration have been recognized during development, in which long-distance tangential migration precedes radial migration of individual cells. Microglial cells moving through the nervous parenchyma are ameboid microglia, which apparently di erentiate into rami®ed microglia after reaching their de®nitive location. This is supported by the presence of cells showing intermediate features between those of ameboid and rami®ed microglia. The factors that control the invasion of the nervous parenchyma, migration within the developing CNS and di erentiation of microglial cells are not well known. These phenomena apparently depend on environmental factors such as soluble or cell-surface bound molecules and components of the extracellular matrix. Microglial cells within the developing CNS are involved in clearing cell debris and withdrawing misdirected or transitory axons, and presumably support cell survival and neurite growth. #

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“…In contrast, microglia are considered "resting" cells that need to be activated to manifest their full potential. This functional difference may explain why perivascular macrophages are continuously replenished by circulating monocytes, whereas microglia turn over very slowly, if at all, under normal conditions (Matsumoto and Fujiwara, 1987;Hickey and Kimura, 1988;Hickey et al, 1992;Lassmann et al, 1993;Bechmann et al, 2001a,b;Vallières and Sawchenko, 2003). Nevertheless, a significant number of microglia can be replaced by monocytes in response to injury or disease (Popovich and Hickey, 2001;Priller et al, 2001;McMahon et al, 2002;Kokovay and Cunningham, 2005;Ladeby et al, 2005;Schilling et al, 2005;Simard et al, 2006;Remington et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Rod-Shaped Monocytes Patrol the Brain Vasculature and Give Rise to Perivascular Macrophages under the Influence of Proinflammatory Cytokines and Angiopoietin-2

Audoy-Rémus¹,

Richard²,

Soulet³

et al. 2008

J. Neurosci.

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The nervous system is constantly infiltrated by blood-derived sentinels known as perivascular macrophages. Their immediate precursors have not yet been identified in situ and the mechanism that governs their recruitment is mostly unknown. Here, we provide evidence that CD68 ϩ GR1 Ϫ monocytes can give rise to perivascular macrophages in mice suffering from endotoxemia. After adhesion to the endothelium, these monocytes start to crawl, adopt a rod-shaped morphology when passing through capillaries, and can manifest the ability to proliferate and form a long cytoplasmic protuberance. They are attracted in greater numbers during endotoxemia by a combination of vasoregulatory molecules, including TNF (tumor necrosis factor), interleukin-1␤, and angiopoietin-2. After a period of several hours, some of them cross the endothelium to expand the population of perivascular macrophages. Depletion of adherent monocytes and perivascular macrophages can be achieved by injection of anti-angiopoietin-2 peptide-Fc fusion protein. This study extends our understanding of the behavior of monocytes at the blood-brain interface and provides a way to block their infiltration into the nervous tissue under inflammatory conditions.

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Absence of donor-type major histocompatibility complex class I antigen-bearing microglia in the rat central nervous system of radiation bone marrow chimeras

Cited by 111 publications

References 19 publications

The cellular response in neuroinflammation: The role of leukocytes, microglia and astrocytes in neuronal death and survival

The cellular response in neuroinflammation: The role of leukocytes, microglia and astrocytes in neuronal death and survival

The origin and differentiation of microglial cells during development

Rod-Shaped Monocytes Patrol the Brain Vasculature and Give Rise to Perivascular Macrophages under the Influence of Proinflammatory Cytokines and Angiopoietin-2

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