Control of myeloid activity during retinal inflammation

Journal of Leukocyte Biology

Andrew D. Dick¹  Debra Carter¹  Edward Hughes¹  John V. Forrester³  Morag Robertson³  Cathryn Broderick²  Janet Liversidge³ 

[1] Division of Ophthalmology, University of Bristol, United Kingdom; Division of Ophthalmology, University of Bristol, United Kingdom; Division of Ophthalmology, University of Bristol, United Kingdom;;Institute of Ophthalmology, University College London, United Kingdom Institute of Ophthalmology, University College London, United Kingdom Institute of Ophthalmology, University College London, United Kingdom;Department of Ophthalmology, University of Aberdeen, United Kingdom; and Department of Ophthalmology, University of Aberdeen, United Kingdom; and Department of Ophthalmology, University of Aberdeen, United Kingdom; and

关键词: macrophages;    microglia;    CD200;    sialoadhesin;   

DOI  :  10.1189/jlb.1102535

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

Combating myeloid cell-mediated destruction of the retina during inflammation or neurodegeneration is dependent on the integrity of homeostatic mechanisms within the tissue that may suppress T cell activation and their subsequent cytokine responses, modulate infiltrating macrophage activation, and facilitate healthy tissue repair. Success is dependent on response of the resident myeloid-cell populations [microglia (MG)] to activation signals, commonly cytokines, and the control of infiltrating macrophage activation during inflammation, both of which appear highly programmed in normal and inflamed retina. The evidence that tissue CD200 constitutively provides down-regulatory signals to myeloid-derived cells via cognate CD200-CD200 receptor (R) interaction supports inherent tissue control of myeloid cell activation. In the retina, there is extensive neuronal and endothelial expression of CD200. Retinal MG in CD200 knockout mice display normal morphology but unlike the wild-type mice, are present in increased numbers and express nitric oxide synthase 2, a macrophage activation marker, inferring that loss of CD200 or absent CD200R ligation results in “classical” activation of myeloid cells. Thus, when mice lack CD200, they show increased susceptibility to and accelerated onset of tissue-specific autoimmunity.

【 授权许可】

Unknown