Elsevier

Clinical Immunology

Volume 101, Issue 3, December 2001, Pages 328-334
Clinical Immunology

Regular Article
CD200 Immunoadhesin Suppresses Collagen-Induced Arthritis in Mice

https://doi.org/10.1006/clim.2001.5117Get rights and content

Abstract

DBA/1 mice immunized with 100 μg bovine collagen type II emulsified in Freund's adjuvant, followed by booster injection in incomplete adjuvant at 18 days, develop profound arthritis (>50% of animals) by 30 days postinjection. The molecule CD200 (previously called OX2), associated with, among others, follicular dendritic cells, is implicated in delivery of immunosuppressive signals to the immune system, and an immunoadhesin in which the extracellular domains of CD200 were linked to a mouse IgG2a Fc region has been shown to promote renal allograft survival. DBA/1 mice receiving 15 μg/mouse CD200Fc at 3-day intervals following immunization with collagen did not develop arthritis in this model. Lymphocytes taken from CD200Fc-treated, collagen-immunized mice produced significantly lower levels of TNFα and IFN-γ in culture supernatants after restimulation in vitro with collagen, in contrast to cells taken from control mice treated with PBS or normal mouse Ig. Serum from CD200Fc-treated mice contained less anti-collagen IgG (∼50% reduction), with relatively more IgG2b and IgG3, and lower levels of TNFα and IFN-γ, than control mice. These data indicate that this immunoadhesin may have a potent role to play in the regulation of autoimmune disorders.

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    Likewise, in cultured retinal myeloid cells from CD200-deficient mice with experimental autoimmune uveoretinitis (EAU), an augmented NO-microglial production was detected on IFNγ addition (Copland et al., 2007). Another experimental test showing more data on the effect of CD200 revealed that activation of CD200R1 with CD200Fc –a soluble recombinant immunoadhesin frequently used to activate CD200R (Gorczynski et al., 2001a; 2001b)–, in LPS-stimulated retinal microglial cultures, inhibits the production of pro-inflammatory mediators through a decrease in the transcription of NF-κB (Copland et al., 2007; Costello et al., 2011; Denieffe et al., 2013; Jiang et al., 2016). Moreover, a recent report demonstrated that the addition of CD200 to microglial cultures exposed to MPP+ (1-methyl-4-phenylpyridinium) inhibited ATP release (Ren et al., 2016).

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    It is apparent that gene-specific siRNAs for POTEA led to attenuation of expression of this TF, and simultaneously to decreased proliferation in treated CLL cells. There are now abundant studies which have documented a role for the CD200:CD200R axis in regulation of inflammation, acquired immunity and cancer biology [1,17,18]. Based on the structure of CD200, with a prominent extracellular V + C domain, a small transmembrane domain with no signaling motifs and no docking sites for adapter signaling molecules, and a short cytoplasmic tail lacking signaling motifs, it had been prevailing dogma that signaling by CD200 occurred through engagement of its extracellular V + C region with a receptor (CD200R) present on other cells [19].

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1

To whom correspondence should be addressed at CCRW 2-855, The Toronto Hospital, 200 Elizabeth Street, Toronto, Ontario M5G 2C4, Canada.

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