From bone marrow to microglia: barriers and avenues

Davoust, Nathalie; Vuaillat, Carine; Androdias, Géraldine; Nataf, Serge

doi:10.1016/j.it.2008.01.010

Cited by 149 publications

(122 citation statements)

References 93 publications

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“…All ␤-gal ϩ cells in this region were immunoreactive for three different antigens expressed in microglia in the developing and mature nervous system, such as F4/80, CD11b, and Iba1 (Davoust et al, 2008;Ginhoux et al, 2010) (Fig. 3B-M ).…”

Section: -L) Together These Results Demonstrate Thatmentioning

confidence: 95%

Regulation of Postnatal Forebrain Amoeboid Microglial Cell Proliferation and Development by the Transcription Factor Runx1

et al. 2012

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Microglia are the immune cells of the nervous system, where they act as resident macrophages during inflammatory events underlying many neuropathological conditions. Microglia derive from primitive myeloid precursors that colonize the nervous system during embryonic development. In the postnatal brain, microglia are initially mitotic, rounded in shape (amoeboid), and phagocytically active. As brain development proceeds, they gradually undergo a transition to a surveillant nonphagocytic state characterized by a highly branched (ramified) morphology. This ramification process is almost recapitulated in reverse during the process of microglia activation in the adult brain, when surveillant microglia undergo a ramified-to-amoeboid morphological transformation and become phagocytic in response to injury or disease. Little is known about the mechanisms controlling amoeboid microglial cell proliferation, activation, and ramification during brain development, despite the critical role of these processes in the establishment of the adult microglia pool and their relevance to microglia activation in the adult brain. Here we show that the mouse transcription factor Runx1, a key regulator of myeloid cell proliferation and differentiation, is expressed in forebrain amoeboid microglia during the first two postnatal weeks. Runx1 expression is then downregulated in ramified microglia. Runx1 inhibits mouse amoeboid microglia proliferation and promotes progression to the ramified state. We show further that Runx1 expression is upregulated in microglia following nerve injury in the adult mouse nervous system. These findings provide insight into the regulation of postnatal microglia activation and maturation to the ramified state and have implications for microglia biology in the developing and injured brain.

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Section: -L) Together These Results Demonstrate Thatmentioning

confidence: 95%

Regulation of Postnatal Forebrain Amoeboid Microglial Cell Proliferation and Development by the Transcription Factor Runx1

et al. 2012

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“…This typical appearance, which is quite different from a classical macrophage, has been associated with microglial "resting" state. Infection, trauma, ischemia, neurodegenerative diseases, or altered neuronal activity, that is any disturbance or loss of brain homeostasis indicating real or potential danger to the CNS can evoke rapid and profound changes in the microglial cell shape, gene expression and the functional behavior which summarily is defined as "microglial activation" (72,169,192,334,351,479,869,949). Phenotypically, the complexity of the cellular processes is reduced, and microglia revert to an amoeboid appearance (Fig.…”

Section: Microglia: From the Warden (Survelliance) To Cleaner (Mamentioning

confidence: 99%

“…The stages of microglial activation were defined based on morphological, molecular, and functional characteristics, with fully activated microglia presenting themselves like other macrophages (169,192,351). Yet these cells are embedded in a specialized tissue (brain parenchyma) which also has to protect itself from the potentially damaging consequences of an immune reaction.…”

Section: Microglia: From the Warden (Survelliance) To Cleaner (Mamentioning

confidence: 99%

“…Regional heterogeneity and populational segregation of microglia in tissues and preparations were demonstrated by morphology, selective detection of constitutive or inducible mRNAs and proteins [e.g., for TNF-␣, IL-6, IGF-I, integrins, CD4, CD11c, CD34, CD40, CD45, CD86, major histocompatibility complex (MHC) class II, Fc␥RII, iNOS, and members of the neurotrophin family], or differences in the proliferative potential (6,111,128,192,247,287,327,351,438,475,485,487,488,552,755,809,810,825,854,872,993). Heterogeneity was also observed in microglia from the aging brain where surprising differences between individuals were found (579,834).…”

Section: Microglia: From the Warden (Survelliance) To Cleaner (Mamentioning

confidence: 99%

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Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,134

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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“…6,22,31,56 However, activated microglia can alter the expression of these molecules as well as their morphology, making differentiation from perivascular cells or blood-derived macrophages difficult or impossible with these techniques. 18 Microglia and macrophage infiltration has been documented in brain tumors in both experimental animal models and human patients, 5,25,72 including meningiomas. 3,8,51 However, the role of these cells is unclear and continues to be debated.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Immune Cell Infiltration Into Canine Intracranial Meningiomas

et al. 2011

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Meningiomas are the most common intracranial tumors in dogs. A variety of inflammatory cells have been shown to invade these tumors in people, but little is known about interactions between the immune system and naturally occurring brain tumors in dogs. The purpose of this study was to investigate the presence of a variety of immune cell subsets within canine intracranial meningiomas. Twenty-three formalin-fixed, paraffin-embedded tumor samples were evaluated using immunohistochemistry with antibodies specific for CD3, CD79a, CD18, CD11d (aD), CD45RA, forkhead box P3, and Toll-like receptors 4 and 9. Immune cell infiltration was evident in all samples, with a predominance of CD3 þ T cells. Large numbers of CD18 þ microglia and macrophages were noted surrounding and infiltrating the tumors, and a subset of these cells within the tumor appeared to be CD11d

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From bone marrow to microglia: barriers and avenues

Cited by 149 publications

References 93 publications

Regulation of Postnatal Forebrain Amoeboid Microglial Cell Proliferation and Development by the Transcription Factor Runx1

Regulation of Postnatal Forebrain Amoeboid Microglial Cell Proliferation and Development by the Transcription Factor Runx1

Physiology of Microglia

Characterization of Immune Cell Infiltration Into Canine Intracranial Meningiomas

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