Down-regulation of the macrophage lineage through interaction with OX2 (CD200).
By R. Hoek, S. Ruuls, C. Murphy, G. J. Wright, R. Goddard, S. Zurawski, B. Blom, M. Homola, Wolfgang Streit, M. Brown and 2 more. Science, 2000
1,070 citations recorded by the source corpus.
Subfields: Immunology, Neurology
View Paper: https://www.semanticscholar.org/paper/c9982ba8bec9bc5e7a3fb39f90f0032dde7c1339
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In Immunology
In Neurology
Citations in the corpus
- Microglia as a source and target of cytokines (2002, background): “The neuronal/endothelial/lymphoid glycoprotein CD200 constitutively provides an inhibitory influence on macrophages/microglia (Hoek et al., 2000; Wright et al., 2000).”
- Microglia as neuroprotective, immunocompetent cells of the CNS (2002, background): “…in the identification of both membrane-bound and secreted factors, such as OX2, neurotrophins, and cytokines/ chemokines, which have the potential for controlling endogenous immune activity within the CNS (Neumann et al., 1998; Harrison et al., 1998; Hoek et al., 2000; Streit et al., 2000, 2001).”
- Points of control in inflammation (2002, background): “In another set of examples, mice lacking the cell-surface immunoglobulin superfamily molecule CD200 suffer more macrophage influx and worse experimental autoimmune encephalomyelitis and collagen-induced arthritis than do wild-type mic”
- The immunology of stroke: from mechanisms to translation (2011, background): “For example, CD200, a surface protein expressed in neurons, interacts with its receptor CD200R on microglia, enforcing a resting phenotyp”
- Control of microglial neurotoxicity by the fractalkine receptor (2006, background): “Mice deficient for CD200, a neuronal glycoprotein whose receptor, CD200R, is expressed by all myeloid cells, show aberrant microglial physiology including morphological activation of microglia in the resting CNS and accelerated response to facial nerve transectio”
- Protective and pathogenic functions of macrophage subsets (2011, background): “Moreover, a subset of macrophages expressing the inhibitory receptor CD200 (also known as OX2) has also been shown to prevent the onset of EAE in mic”
- The biphasic function of microglia in ischemic stroke (2017, positive): “Deficiency of CD200 or blockade of CD200R in mice led to enhanced microglia activation and worsened symptoms in the mouse model of EAE, facial nerve transection, retinal inflammation, and encephalitis (Broderick et al., 2002; Deckert et al., 2006; Hoek et al., 2000).”
- Microglial Activation & Chronic Neurodegeneration (2010, background): “In addition, the expression of certain receptors, such as CD200 and CX3CR1 on the microglia cell surface, may interact with ligands that keep microglia in a resting state.(20,21) Resting, ramified, microglia cell bodies are spaced throughout the CNS to avoid cell body overlap, but have been shown to”
- Macrophages: development and tissue specialization. (2015, background): “Neuronal CX3CL1, CD200, and exosome-derived miR-124 were shown to control microglial cell-autonomous neurotoxicity in various CNS inflammation models (132, 133, 182).”
- Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. (2012, positive): “In the healthy brain neurons express a number of immunosuppressive proteins such as CD200, CD47 and fractalkine, which interact with their receptors on microglia to maintain the microglia in a quiescent/non-activated state (Harrison et al., 1998; Hoek et al., 2000; Lynch, 2009).”
- T Follicular Helper Cells Express a Distinctive Transcriptional Profile, Reflecting Their Role as Non-Th1/Th2 Effector Cells That Provide Help for B Cells1 (2004, background): “CD200 is a member of the Ig superfamily (44, 45), and its receptor is reported to be a myeloidspecific glycoprotein CD200R (44).”
- Microglia, major player in the brain inflammation: their roles in the pathogenesis of Parkinson's disease (2006, background): “In CD200 knock out mice, microglia were spontaneously activated as determined by increased CD11b and CD45 as well as by loss of their ramified morphology (Hoek et al., 2000).”