ArticleJournal of immunology (Baltimore, Md. : 1950)2005
Enhanced tolerance to autoimmune uveitis in CD200-deficient mice correlates with a pronounced Th2 switch in response to antigen challenge.
Article in Journal of immunology (Baltimore, Md. : 1950), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Understanding the squamous cell carcinoma immune microenvironment.Frontiers in immunology · 2023Review
- Article
- Upregulated CD200 in pre-retinal proliferative fibrovascular membranes of proliferative diabetic retinopathy patients and its correlation with vascular endothelial growth factor.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- Article
- Autoimmune and autoinflammatory mechanisms in uveitis.Seminars in immunopathology · 2014Review
- CD200-CD200R signaling suppresses anti-tumor responses independently of CD200 expression on the tumor.Oncogene · 2012Article
- CD200-CD200R dysfunction exacerbates microglial activation and dopaminergic neurodegeneration in a rat model of Parkinson's disease.Journal of neuroinflammation · 2011Article
- Article
- Monoclonal antibody-mediated CD200 receptor signaling suppresses macrophage activation and tissue damage in experimental autoimmune uveoretinitis.The American journal of pathology · 2007Article
- Identification of novel dendritic cell populations in normal mouse retina.Investigative ophthalmology & visual science · 2007Article
- Is the CD200/CD200 receptor interaction more than just a myeloid cell inhibitory signal?Critical reviews in immunology · 2006Review
- Immunohistochemical Expression of CD200 in Renal Cell Carcinoma.Journal of microscopy and ultrastructureArticle
Corrections and comments
- Erratum issuedMcConnachie, Karen [corrected to McConachie, Karen]
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
A single exposure to inhaled Ag 10 days before immunization leads to long term, Ag-specific tolerance. Respiratory tract myeloid APCs are implicated, but how regulation is invoked, and how tolerance is sustained are unclear. This study examines the in vivo function of the myeloid regulatory molecule CD200 in the process of tolerance induction. Despite earlier onset of experimental autoimmune uveitis in sham-tolerized, CD200-deficient mice, disease incidence and subsequent severity were actually reduced compared with those in wild-type mice. Protection was more effective and long term, lasting at least 28 days. Halting disease progression and tolerance in CD200(-/-) mice correlated with a marked increase in Th2-associated cytokine production by Ag-challenged splenocytes. Reduced overall disease and enhanced tolerance in the CD200-deficient mice in this model system were unexpected and may be related to altered populations of MHC class II(low) APC in the respiratory tract compared with wild-type mice together with associated activation of STAT6 in draining lymph nodes of tolerized mice. These data indicate that in the absence of default inhibitory CD200 receptor signaling, alternative, powerful regulatory mechanisms are invoked. This may represent either permissive dominant Th2 activation or an altered hierarchy of negative signaling by other myeloid cell-expressed regulatory molecules.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.