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Blocking CD200-CD200 receptor axis augments NOS-2 expression and aggravates experimental autoimmune uveoretinitis in
Debatri Banerjee1, Andrew D Dick
1Department of Ophthalmology, University of Bristol, UK.
Purpose:
Tissue expression of CD200 generates inhibitory or down-regulatory signals to macrophages and microglia within CNS and retina. Our interests were to investigate whether blocking CD200 receptor (CD200R) signalling in vivo results in macrophage activation and thus aggravation of EAU in Lewis rats.
Methods:
Retinal extract-immunised Lewis rats were treated day 3 and 5 post-immunisation with CD200R mAb or normal mouse serum. Phenotypic analysis of the leucocyte infiltrate and disease severity was clinically and histogically examined.
Results:
Rats administered with CD200R mAb developed earlier onset of EAU and more severe disease. Blocking CD200R increased retinal neuronal CD200 expression and, although disease severity was increased concomitant with an increase in NOS-2 expression, retinal macrophage numbers were not increased.
Conclusions:
Contemporaneous with data from CD200KO mice, these results support the notion that CD200-CD200R signalling suppresses macrophage activation. Exacerbation of EAU in both CD200KO mice and Lewis rats when CD200-CD200R interaction is blocked suggests that this could be an avenue for therapeutic intervention.
Insights
Blocking the CD200 receptor (CD200R) in rats aggravated experimental autoimmune uveitis (EAU). This suggests the CD200-CD200R pathway normally suppresses macrophage activation, offering a potential therapeutic target for EAU.
Area of Science:
- Immunology
- Neuroscience
- Ophthalmology
Background:
- CD200 expressed in tissues sends inhibitory signals to macrophages and microglia.
- The CD200-CD200R pathway's role in autoimmune diseases like EAU is not fully understood.
Purpose of the Study:
- To investigate if blocking CD200 receptor (CD200R) signaling in vivo exacerbates experimental autoimmune uveitis (EAU) in Lewis rats.
- To determine if CD200R blockade leads to macrophage activation and increased disease severity.
Main Methods:
- Lewis rats were immunized with retinal extract and treated with CD200R monoclonal antibody (mAb) or normal mouse serum.
- Leukocyte infiltrate and disease severity were assessed clinically and histologically.
Main Results:
- CD200R mAb treatment resulted in earlier onset and more severe EAU.
- Blocking CD200R increased neuronal CD200 expression and NOS-2, but not macrophage numbers.
- Disease exacerbation correlated with increased NOS-2 expression.
Conclusions:
- CD200-CD200R signaling suppresses macrophage activation, as evidenced by EAU exacerbation upon blockade.
- Blocking this interaction in CD200 knockout mice and Lewis rats supports its suppressive role.
- The CD200-CD200R pathway represents a potential therapeutic target for autoimmune diseases like EAU.
