Modulation (Inhibition and Augmentation) of Complement Receptor-3-Mediated Myelin Phagocytosis

Reichert, Fanny; Slobodov, Uri; Makranz, Chen; Rotshenker, Shlomo

doi:10.1006/nbdi.2001.0383

Cited by 39 publications

(41 citation statements)

References 46 publications

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“…For example, in models of SCI where acute inflammation has neurotoxic effects, anti-integrin antibodies (e.g., α D β 2 or α 4 β 1 ) confer neuroprotection and improve recovery of function (Yip et al 1998;Yip and Siu 2001;Bao et al 2004;Gris et al 2004;Pittier et al 2005;Fleming et al 2008Fleming et al , 2009Bao et al 2011). Activation of other integrins (α M β 2 /Mac-1) expressed on the surface of microglia and macrophages could improve axon regeneration indirectly by enhancing phagocytic clearance of myelin debris (Brück and Friede 1990;Reichert et al 2001;Rotshenker 2003;Mukaino et al 2010).…”

Section: Integrinsmentioning

confidence: 99%

“…It can inhibit macrophage proliferation and cytokine release (Schimizzi et al 2006;Taylor et al 2007;Gardiner 2011). However, hydrogels composed of HMW HA reduce synthesis of CSPGs by astrocytes and have been shown to be anti-inflammatory in models of SCI (Brück and Friede 1990;Reichert et al 2001;Rotshenker 2003;Yasuda 2007;Khaing et al 2011). HA also acts directly on neurons.…”

Section: Introductionmentioning

confidence: 97%

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Achieving CNS axon regeneration by manipulating convergent neuro-immune signaling

et al. 2012

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After central nervous system (CNS) trauma, axons have a low capacity for regeneration. Regeneration failure is associated with a muted regenerative response of the neuron itself, combined with a growth-inhibitory and cytotoxic post-injury environment. After spinal cord injury (SCI), resident and infiltrating immune cells (especially microglia/macrophages) contribute significantly to the growth-refractory milieu near the lesion. By targeting both the regenerative potential of the axon and the cytotoxic phenotype of microglia/macrophages, we may be able to improve CNS repair after SCI. In this review, we discuss molecules shown to impact CNS repair by affecting both immune cells and neurons. Specifically, we provide examples of pattern recognition receptors, integrins, cytokines/chemokines, nuclear receptors and galectins that could improve CNS repair. In many cases, signaling by these molecules is complex and may have contradictory effects on recovery depending on the cell types involved or the model studied. Despite this caveat, deciphering convergent signaling pathways on immune cells (which affect axon growth indirectly) and neurons (direct effects on axon growth) could improve repair and recovery after SCI. Future studies must continue to consider how regenerative therapies targeting neurons impact other cells in the pathological CNS. By identifying molecules that simultaneously improve axon regenerative capacity and drive the protective, growth-promoting phenotype of immune cells, we may discover SCI therapies that act synergistically to improve CNS repair and functional recovery.

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Section: Integrinsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Achieving CNS axon regeneration by manipulating convergent neuro-immune signaling

et al. 2012

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“…However, the presence of complement improved myelin uptake [138]. Recent studies have shown that CR3-mediated myelin phagocytosis can be modulated by monoclonal antibodies (mAb) that bind to distinct epitopes of subunits αM and β-2 of CR3.…”

Section: Myelin Phagocytosis By Microglial Cellsmentioning

confidence: 99%

“…This mAb-induced modulation of myelin phagocytosis occurred on the complement-dependent and complement-independent pathways. These results suggest that a direct binding site for myelin exists on CR3 and that this site is probably on αM [138]. In microglial cells, complement receptors are also implicated in the phagocytosis of myelin opsonized with proteins from the complement cascade [139].…”

Section: Myelin Phagocytosis By Microglial Cellsmentioning

confidence: 99%

Phagocytic functions of microglial cells in the central nervous system and their importance in two neurodegenerative diseases: multiple sclerosis and Alzheimer’s disease

Choucair¹,

Laporte

Lévy³

et al. 2006

Open Life Sciences

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Microglial cells are the resident phagocytic cells of the central nervous system (CNS). They possess a wide range of receptors allowing them to identify and internalize numerous pathogens. We will discuss here the role of the most important receptors of microglia involved in non-opsonin-dependent phagocytosis (mannose receptor, β-glucan receptor, scavenger receptor) and that of receptors involved in the opsonin-dependent phagocytosis, namely the complement 3 (CR3) and the Fcγ receptors (FcγR). First, the molecular and cellular mechanisms induced when these receptors are conducting a phagocytic event are presented. In the second part, we will discuss the role these receptors may play in multiple sclerosis and Alzheimer's disease, in the elimination by phagocytosis of myelin and beta amyloid peptide respectively.

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“…Integrins are another group of proteins present in cell membranes that have been shown to mediate some physiological functions of phagocytes (macrophages and polymorphonuclear leukocytes) and could also play a role in pathological conditions (5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Phagocytosis by macrophages mediated by receptors for denatured proteins - dependence on tyrosine protein kinases

Hespanhol

Mantovani

2002

Braz J Med Biol Res

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Previous studies have demonstrated that some components of the leukocyte cell membrane, CR3 (Mac-1, CD11b/CD18) and p150/95, are able to bind to denatured proteins. Thus, it is of interest to know which effector functions of these cells can be triggered by these receptors when they interact with particles or surfaces covered with denatured proteins. In the present study we analyzed their possible role as mediators of phagocytosis of red cells covered with denatured bovine serum albumin (BSA) by mouse peritoneal macrophages. We observed that a) macrophages are able to recognize (bind to) these red cells, b) this interaction can be inhibited by denatured BSA in the fluid phase, c) there is no phagocytosis of these particles by normal macrophages, d) phagocytosis mediated by denatured BSA can be, however, effectively triggered in inflammatory macrophages induced by glycogen or in macrophages activated in vivo with LPS, and e) this phagocytic capacity is strongly dependent on the activity of tyrosine protein kinases in its signal transduction pathway, as demonstrated by using three kinds of enzyme inhibitors (genistein, quercetin and herbimycin A).

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Modulation (Inhibition and Augmentation) of Complement Receptor-3-Mediated Myelin Phagocytosis

Cited by 39 publications

References 46 publications

Achieving CNS axon regeneration by manipulating convergent neuro-immune signaling

Achieving CNS axon regeneration by manipulating convergent neuro-immune signaling

Phagocytic functions of microglial cells in the central nervous system and their importance in two neurodegenerative diseases: multiple sclerosis and Alzheimer’s disease

Phagocytosis by macrophages mediated by receptors for denatured proteins - dependence on tyrosine protein kinases

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