Mice Lacking CD200R1 Show Absence of Suppression of Lipopolysaccharide-Induced Tumor Necrosis Factor-α and Mixed Leukocyte Culture Responses by CD200

Boudakov, Ivo; Liu, Jian; Fan, Na; Gulay, Suna P.; Wong, Karrie; Gorczynski, Reg

doi:10.1097/01.tp.0000269795.04592.cc

Cited by 72 publications

(77 citation statements)

References 24 publications

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“…Homozygous CD200R1KO, CD200 tg , or R1KO ϫ CD200 tg mice or wt controls received C3H skin allografts (30). In some cases, mice received i.v.…”

Section: Skin Allograft Rejection In Vivomentioning

confidence: 99%

“…KO mice have been shown by Southern gel analysis, PCR, and FACS to lack expression of DNA, mRNA, or cell-surface protein, respectively, encoding a full-length CD200R1. Suppression by CD200 of TNF-␣ production in LPS-stimulated cells is abolished in CD200R1KO mice (30). A "second generation" CD200 tg mouse, using a less "leaky" CMV promoter (rtTASM2 (32)), was bred to homozygosity on a wt BL/6 background for these studies, and it was also subsequently crossed to homozygous CD200R1KO mice to produce dual homozygous R1KO ϫ CD200 tg mice.…”

Section: Micementioning

confidence: 99%

“…Mice were used within 2 wk of arrival from the supplier. CD200 tg mice (overexpressing CD200 under control of a doxycyclinesensitive inducer) and CD200R1KO mice (BL/6 background), lacking the extracellular domains of CD200R1, were produced as described elsewhere and maintained in our own animal colony (30,31). KO mice have been shown by Southern gel analysis, PCR, and FACS to lack expression of DNA, mRNA, or cell-surface protein, respectively, encoding a full-length CD200R1.…”

Section: Micementioning

confidence: 99%

“…Using FACS analysis and real-time PCR, neither spleen nor bone marrow cells from CD200R1KO mice expressed mRNA or cell-surface protein for CD200R1, unlike littermate (wild-type, (wt)) controls (30). Given our studies supporting the hypothesis that CD200 triggering of alternate CD200R isoforms (not CD200R1) on DC precursors preferentially led to the induction of "tolerogenic" DCs (29), we designed studies using cells from homozygous CD200R1KO, CD200 tg , and CD200R1KO ϫ CD200 tg mice to investigate this hypothesis.…”

mentioning

confidence: 99%

“…We recently generated a BL/6 mouse with deletion of the exons encoding the extracellular domains of CD200R1 (30), as well as mice overexpressing CD200 under control of a doxycycline-inducible promoter (CD200 tg (31)). Using FACS analysis and real-time PCR, neither spleen nor bone marrow cells from CD200R1KO mice expressed mRNA or cell-surface protein for CD200R1, unlike littermate (wild-type, (wt)) controls (30).…”

mentioning

confidence: 99%

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An Interaction between CD200 and Monoclonal Antibody Agonists to CD200R2 in Development of Dendritic Cells That Preferentially Induce Populations of CD4+CD25+ T Regulatory Cells

Gorczynski

Khatri

Lee

et al. 2008

The Journal of Immunology

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In previous studies we reported that while interaction between the relatively ubiquitously expressed molecule CD200 and one of its receptors, CD200R1, resulted in direct suppression of alloreactivity, engagement of alternate receptors led instead to altered differentiation of dendritic cells (DCs) from marrow precursors, which could in turn foster development of Foxp3+ regulatory T cells. We have explored this effect of engagement of alternate receptors by using a monoclonal agonist Ab to CD200R2 and investigating expression of TLRs on DCs induced in vivo and in vitro after CD200 stimulation in mice in which the gene encoding CD200R1 was deleted. CD200 stimulation was achieved by using either a soluble form of CD200 (CD200Fc) or overexpression of CD200 as a doxycycline-inducible transgene. Although broadly similar effects were seen, consistent with the hypothesis that triggering of CD200R2 does produce DCs with a characteristic TLR repertoire, there are subtle differences in suppression of alloreactivity achieved by CD200 delivered in these two manners, which is consistent with a complexity of CD200:CD200R engagement not previously appreciated.

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“…Homozygous CD200R1KO, CD200 tg , or R1KO ϫ CD200 tg mice or wt controls received C3H skin allografts (30). In some cases, mice received i.v.…”

Section: Skin Allograft Rejection In Vivomentioning

confidence: 99%

Section: Micementioning

confidence: 99%

Section: Micementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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An Interaction between CD200 and Monoclonal Antibody Agonists to CD200R2 in Development of Dendritic Cells That Preferentially Induce Populations of CD4+CD25+ T Regulatory Cells

Gorczynski

Khatri

Lee

et al. 2008

The Journal of Immunology

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CD33 and CD33-Related Siglecs in Pathogen Recognition and Endocytosis of DC in the Innate Immune System

Kim

2022

Glycobiology of Innate Immunology

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The Classification of Microglial Activation Phenotypes on Neurodegeneration and Regeneration in Alzheimer’s Disease Brain

Varnum

Ikezu

2012

Arch. Immunol. Ther. Exp.

332

252

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Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive decline of cognitive function and memory formation. There is no therapeutic that can halt or reverse its progression. Contemporary research suggests that age-dependent neuroinflammatory changes may play a significant role in the decreased neurogenesis and cognitive impairments in AD. The innate immune response is characterized by pro-inflammatory (M1) activation of macrophages and subsequent production of specific cytokines, chemokines, and reactive intermediates, followed by resolution and alternative activation for anti-inflammatory signaling (M2a) and wound healing (M2c). We propose that microglial activation phenotypes are analogous to those of macrophages and that their activation plays a significant role in regulating neurogenesis in the brain. Microglia undergo a switch from an M2- to an M1-skewed activation phenotype during aging. This review will assess the neuroimmunological studies that led to characterization of the different microglial activation states using AD mouse models. It will also discuss the roles of microglial activation on neurogenesis in AD and propose anti-inflammatory molecules as exciting therapeutic targets for research. Molecules like interleukin-4 and CD200 have proven to be important anti-inflammatory molecules in the regulation of neuroinflammation in the brain, and they will be discussed in detail for their therapeutic potential.

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Mice Lacking CD200R1 Show Absence of Suppression of Lipopolysaccharide-Induced Tumor Necrosis Factor-α and Mixed Leukocyte Culture Responses by CD200

Abstract: CD200:CD200R1 plays an immunoregulatory role in vivo.

Cited by 72 publications

References 24 publications

An Interaction between CD200 and Monoclonal Antibody Agonists to CD200R2 in Development of Dendritic Cells That Preferentially Induce Populations of CD4+CD25+ T Regulatory Cells

An Interaction between CD200 and Monoclonal Antibody Agonists to CD200R2 in Development of Dendritic Cells That Preferentially Induce Populations of CD4+CD25+ T Regulatory Cells

CD33 and CD33-Related Siglecs in Pathogen Recognition and Endocytosis of DC in the Innate Immune System

The Classification of Microglial Activation Phenotypes on Neurodegeneration and Regeneration in Alzheimer’s Disease Brain

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