The CD200 Receptor Is a Novel and Potent Regulator of Murine and Human Mast Cell Function

Cherwinski, Holly; Murphy, Craig A.; Joyce, Barbara; Bigler, Mike; Song, Yali; Zurawski, Sandra; Moshrefi, Mehrdad; Gorman, Daniel M.; Miller, Kathy; Zhang, Shuli; Sedgwick, JD; Phillips, Joseph H.

doi:10.4049/jimmunol.174.3.1348

Cited by 108 publications

(105 citation statements)

References 53 publications

Supporting

Mentioning

100

Contrasting

Order By: Relevance

“…3 A, B, available at www.jneurosci.org as supplemental material). Previous studies have shown that CD200 engagement with its receptor downregulates inflammation; thus, administration of a CD200 fusion protein ameliorated changes observed in collagen-induced arthritis (Gorczynski et al, 2002), and CD200 -CD200R interaction has also been reported to prevent degranulation and cytokine release from mast cells (Cherwinski et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

CD200 Ligand–Receptor Interaction Modulates Microglial ActivationIn VivoandIn Vitro: A Role for IL-4

Lyons¹,

Downer²,

Crotty³

et al. 2007

J. Neurosci.

229

242

View full text Add to dashboard Cite

Deficits in cognitive function are associated with neuroinflammatory changes, typified by activation of glial cells and an alteration of the pro-and anti-inflammatory cytokine balance in the brain. Although there is evidence to suggest that activation of microglia is regulated by interaction with other cell types in the brain, the mechanism(s) involved is poorly understood. Here, we provide evidence that interaction between CD200 and its receptor plays a role in modulating microglial activation under conditions of chronic and acute inflammation of the brain. We report that interleukin-4 (IL-4) plays a central role in modulating expression of CD200 and identify a mechanism by which IL-4 directly controls microglial cell activation. Our findings provide the first demonstration of a role for IL-4 in modulating CD200 expression and suggest a mechanism for regulation of microglial activation in the intact CNS under inflammatory conditions.

show abstract

Section: Discussionmentioning

confidence: 99%

CD200 Ligand–Receptor Interaction Modulates Microglial ActivationIn VivoandIn Vitro: A Role for IL-4

Lyons¹,

Downer²,

Crotty³

et al. 2007

J. Neurosci.

229

242

View full text Add to dashboard Cite

show abstract

“…In vitro studies have shown that ligation of CD200R results in decreased degranulation and cytokine secretion by mast cells, monocytes and macrophages (Jenmalm et al, 2006;Cherwinski et al, 2005). In addition, deletion of the CD200 gene in mice results in enhanced susceptibility to auto-immune disease and increased myeloid response to inflammation .…”

Section: E-mail Address: Lmeyaard@umcutrechtnl (L Meyaard)mentioning

confidence: 99%

The inhibitory CD200R is differentially expressed on human and mouse T and B lymphocytes

Rijkers

Ruiter

Baridi

et al. 2008

Molecular Immunology

118

View full text Add to dashboard Cite

To ensure an adequate response against pathogens and prevent unwanted self-reactivity, immune cells need to functionally express both activating and inhibitory receptors. CD200R is an inhibitory receptor mainly expressed on myeloid cells that down-modulates cellular activation both in vivo and in vitro. Although previously mainly studied as a regulator of myeloid function, we now show that CD200R is differentially expressed on human and mouse T-cell subsets. In both species, CD4 + T cells express higher amounts of CD200R than CD8 + T cells, and memory cells express higher amounts of CD200R than naïve or effector cells. CD200R expression is up-regulated on both CD4 + and CD8 + T cells after stimulation in vitro. Furthermore, we show CD200R expression on human and mouse B cells. In human tonsils, CD200R is differentially expressed on B cells, with high expression on memory cells and plasmablasts. Mice lacking the ligand for CD200R, CD200 −/− mice, do not show abnormal composition of the lymphocyte compartment and have normal B cell responses to antigenic challenge. Although the functional implications remain to be elucidated, the expression of CD200R on lymphocytes suggests a much broader role for CD200R-mediated immune regulation than previously anticipated.

show abstract

“…14,15 If we attempt to reconstitute and de-activate macrophage function (by direct ligation of CD200R with anti-CD200R monoclonal antibodies or by a CD200Fc), attenuation of retinal or CNS inflammation can be achieved 14,16 as well as regulation of other myeloid cells, including mast cells in the lung. [17][18][19][20] How do we keep the peace? A premise lies that there is continual immunosurveillance, akin to CNS, and that alongside the immune cell inhabitants of the retina and choroid, together achieve constant sensing to respond to danger signals.…”

Section: Keeping the Peacementioning

confidence: 99%

Doyne lecture 2016: intraocular health and the many faces of inflammation

Dick

2016

Eye

View full text Add to dashboard Cite

Dogma for reasons of immune privilege including sequestration (sic) of ocular antigen, lack of lymphatic and immune competent cells in the vital tissues of the eye has long evaporated. Maintaining tissue and cellular health to preserve vision requires active immune responses to prevent damage and respond to danger. A priori the eye must contain immune competent cells, undergo immune surveillance to ensure homoeostasis as well as an ability to promote inflammation. By interrogating immune responses in non-infectious uveitis and compare with age-related macular degeneration (AMD), new concepts of intraocular immune health emerge. The role of macrophage polarisation in the two disorders is a tractable start. TNF-alpha regulation of macrophage responses in uveitis has a pivotal role, supported via experimental evidence and validated by recent trial data. Contrast this with the slow, insidious degeneration in atrophic AMD or in neovasular AMD, with the compelling genetic association with innate immunity and complement, highlights an ability to attenuate pathogenic immune responses and despite known inflammasome activation. Yolk sac-derived microglia maintains tissue immune health. The result of immune cell activation is environmentally dependent, for example, on retinal cell bioenergetics status, autophagy and oxidative stress, and alterations that skew interaction between macrophages and retinal pigment epithelium (RPE). For example, dead RPE eliciting macrophage VEGF secretion but exogenous IL-4 liberates an anti-angiogenic macrophage sFLT-1 response. Impaired autophagy or oxidative stress drives inflammasome activation, increases cytotoxicity, and accentuation of neovascular responses, yet exogenous inflammasome-derived cytokines, such as IL-18 and IL-33, attenuate responses.

show abstract

The CD200 Receptor Is a Novel and Potent Regulator of Murine and Human Mast Cell Function

Cited by 108 publications

References 53 publications

CD200 Ligand–Receptor Interaction Modulates Microglial ActivationIn VivoandIn Vitro: A Role for IL-4

CD200 Ligand–Receptor Interaction Modulates Microglial ActivationIn VivoandIn Vitro: A Role for IL-4

The inhibitory CD200R is differentially expressed on human and mouse T and B lymphocytes

Doyne lecture 2016: intraocular health and the many faces of inflammation

Contact Info

Product

Resources

About