Repertoire of microglial and macrophage responses after spinal cord injury

David, Samuel; Kroner, Antje

doi:10.1038/nrn3053

Cited by 1,168 publications

(1,113 citation statements)

References 163 publications

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“…This subset expresses CD16, CD32, CD86, major histocompatibility complex (MHC) II, and inducible nitric oxide synthase (iNOS). Alternatively activated (M2) mononuclear phagocytes function in wound healing and repair through phagocytosis and immune tolerance [103]. The M2 cells are further divided into M2a, M2b, and M2c subtypes [103][104][105].…”

Section: Phenotype Of Mononuclear Phagocytesmentioning

confidence: 99%

“…Alternatively activated (M2) mononuclear phagocytes function in wound healing and repair through phagocytosis and immune tolerance [103]. The M2 cells are further divided into M2a, M2b, and M2c subtypes [103][104][105]. The M2a subset expresses arginase-1, Ym1, and Fizz, and is involved in immunity against parasites, T helper 2 cell recruitment, tissue repair, and growth stimulation.…”

Section: Phenotype Of Mononuclear Phagocytesmentioning

confidence: 99%

“…This subset exhibits both pro-and anti-inflammatory features and is associated with adaptive immunity. Arginase-1, CD163, and CD206 are markers for M2c cells, which mainly function in scavenging cell debris during the repair process [9,103]. Apart from M1 and M2 phenotypes, a novel Mox phenotype has been described in atherosclerotic lesions of a hyperlipidemic mouse model.…”

Section: Phenotype Of Mononuclear Phagocytesmentioning

confidence: 99%

“…M1 macrophages release cytotoxic substances, eliciting inflammation and contributing to cell death, while M2 macrophages clear cellular debris through phagocytosis and release trophic factors [103,105]. In the presence of microbes, the acute inflammatory response is often rapid, specific, and self-limiting, to avoid inflammation-mediated damage to neighboring tissues [118].…”

Section: Inflammation Versus Resolutionmentioning

confidence: 99%

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Microglia and Monocyte-Derived Macrophages in Stroke

2016

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Historically, the brain has been considered an immune-privileged organ separated from the peripheral immune system by the blood-brain barrier. However, immune responses do occur in the brain in neurological conditions in which the integrity of the blood-brain barrier is compromised, exposing the brain to peripheral antigens and endogenous danger signals. While most of the associated pathological processes occur in the central nervous system, it is now clear that peripheral immune cells, especially mononuclear phagocytes, that infiltrate into the injury site play a key role in modulating the progression of primary brain injury development. As inflammation is a necessary and critical component for the subsequent injury resolution process, understanding the contribution of mononuclear phagocytes on the regulation of inflammatory responses may provide novel approaches for potential therapies. Furthermore, predisposed comorbid conditions at the time of stroke cause the alteration of stroke-induced immune and inflammatory responses and subsequently influence stroke outcome. In this review, we summarize a role for microglia and monocytes/macrophages in acute ischemic stroke in the context of normal and metabolically compromised conditions.

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Section: Phenotype Of Mononuclear Phagocytesmentioning

confidence: 99%

Section: Phenotype Of Mononuclear Phagocytesmentioning

confidence: 99%

Section: Phenotype Of Mononuclear Phagocytesmentioning

confidence: 99%

Section: Inflammation Versus Resolutionmentioning

confidence: 99%

See 2 more Smart Citations

Microglia and Monocyte-Derived Macrophages in Stroke

2016

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“…There have been a number of studies that demonstrate the beneficial neuroprotective and neuroreparative effects of M2 switching [68][69][70][71]. These studies have focused on the importance of various M2 markers such as IL-4 [72,73], IL-10 [72,74,75], IL-1RA [76], TGF-β [77,78], CD206 [72,79], arginase 1 [79,80], granulocyte macrophage colony-stimulating factor [72], insulin-like growth factor 1 [81,82], and peroxisome proliferator-activated receptor-γ [70,71,83]. Even though our understanding of the role of these individual factors have become more insightful, it is very difficult to achieve beneficial neuroprotective effects by modulating just one of these factors.…”

Section: Targeting Microglia As a Therapeutic Strategymentioning

confidence: 99%

Is Immunomodulation a Principal Mechanism Underlying How Cell-Based Therapies Enhance Stroke Recovery?

Satani

Savitz

2016

Neurotherapeutics

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Inflammation within the brain and in peripheral tissues contributes to brain injury following ischemic stroke. Therapeutic modulation of the inflammatory response has been actively pursued as a novel stroke treatment approach for decades, without success. In recent years, extensive studies support the high potential for cell-based therapies to become a new treatment modality for stroke and other neurological disorders. In this review, we explore different types of cellular therapies and discuss how they modulate central and peripheral inflammatory processes after stroke. Apart from identifying potential targets for cell therapy, we also discuss paracrine and immunomodulatory mechanisms of cell therapy.

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Biomarker-Based Predictive Models for Prognosis in Amyotrophic Lateral Sclerosis

Simmons

Mitchell

et al. 2013

JAMA Neurol

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IMPORTANCE Although median survival in amyotrophic lateral sclerosis (ALS) is 2 to 4 years, survival ranges from months to decades, creating prognostic uncertainty. Strategies to predict prognosis would benefit clinical management and outcomes assessments of clinical trials. OBJECTIVE To identify biomarkers in plasma and cerebrospinal fluid (CSF) of patients with ALS that can predict prognosis. DESIGN, PARTICIPANTS, AND SETTING We conducted a retrospective study of plasma (n = 29) and CSF (n = 33) biomarkers identified in samples collected between March 16, 2005, and August 22, 2007, from patients with ALS at an academic tertiary care center. Participants included patients who were undergoing diagnostic evaluation in the neurology outpatient clinic and were eventually identified as having definite, probable, laboratory-supported probable, or possible ALS as defined by revised El-Escorial criteria. All were white and none had a family history of ALS. Clinical information extended from initial presentation to death. Genotyping for hemochromatosis (HFE) gene status was performed. Multiplex and immunoassay analysis of plasma and CSF was used to measure levels of 35 biomarkers. Statistical modeling was used to identify biomarker panels that could predict total disease duration. MAIN OUTCOMES AND MEASURES Total disease duration, defined as the time from symptom onset to death, was the main outcome. The hypothesis being tested was formulated after data collection. RESULTS Multivariable models for total disease duration using biomarkers from plasma, CSF, and plasma and CSF combined incorporated 7, 6, and 6 biomarkers to achieve goodness-of-fit R 2 values of 0.769, 0.617, and 0.962, respectively. After classification into prognostic categories, actual and predicted values achieved moderate to good agreement, with Cohen κ values of 0.526, 0.515, and 0.930 for plasma, CSF, and plasma and CSF combined models, respectively. Inflammatory biomarkers, including select interleukins, growth factors such as granulocyte colony-stimulating factor, and L-ferritin, had predictive value. CONCLUSIONS AND RELEVANCE This study provides proof-of-concept for a novel multivariable modeling strategy to predict ALS prognosis. These results support unbiased biomarker discovery efforts in larger patient cohorts with detailed longitudinal follow-up.

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Repertoire of microglial and macrophage responses after spinal cord injury

Cited by 1,168 publications

References 163 publications

Microglia and Monocyte-Derived Macrophages in Stroke

Microglia and Monocyte-Derived Macrophages in Stroke

Is Immunomodulation a Principal Mechanism Underlying How Cell-Based Therapies Enhance Stroke Recovery?

Biomarker-Based Predictive Models for Prognosis in Amyotrophic Lateral Sclerosis

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