Control of myeloid activity during retinal inflammation

A. D. Dick, D. Carter, Marie Robertson, C. Broderick, E. Hughes, John Vincent Forrester, Janet Mary Liversidge

Research output: Contribution to journalEditorial

71 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)161-166
Number of pages5
JournalJournal of Leukocyte Biology
Volume74
Issue number2
DOIs
Publication statusPublished - 2003

Keywords

  • macrophages
  • microglia
  • CD200
  • sialoadhesin
  • EXPERIMENTAL AUTOIMMUNE UVEORETINITIS
  • TUMOR-NECROSIS-FACTOR
  • IMMUNE DEVIATION ACAID
  • II-POSITIVE CELLS
  • ANTIGEN PRESENTATION
  • OX2 GLYCOPROTEIN
  • DENDRITIC CELLS
  • MOLECULAR-BASIS
  • IFN-GAMMA
  • MACROPHAGES

Cite this

Dick, A. D., Carter, D., Robertson, M., Broderick, C., Hughes, E., Forrester, J. V., & Liversidge, J. M. (2003). Control of myeloid activity during retinal inflammation. Journal of Leukocyte Biology, 74(2), 161-166. https://doi.org/10.1189/jlb.1102535

Control of myeloid activity during retinal inflammation. / Dick, A. D.; Carter, D.; Robertson, Marie; Broderick, C.; Hughes, E.; Forrester, John Vincent; Liversidge, Janet Mary.

In: Journal of Leukocyte Biology, Vol. 74, No. 2, 2003, p. 161-166.

Research output: Contribution to journalEditorial

Dick, AD, Carter, D, Robertson, M, Broderick, C, Hughes, E, Forrester, JV & Liversidge, JM 2003, 'Control of myeloid activity during retinal inflammation', Journal of Leukocyte Biology, vol. 74, no. 2, pp. 161-166. https://doi.org/10.1189/jlb.1102535
Dick AD, Carter D, Robertson M, Broderick C, Hughes E, Forrester JV et al. Control of myeloid activity during retinal inflammation. Journal of Leukocyte Biology. 2003;74(2):161-166. https://doi.org/10.1189/jlb.1102535
Dick, A. D. ; Carter, D. ; Robertson, Marie ; Broderick, C. ; Hughes, E. ; Forrester, John Vincent ; Liversidge, Janet Mary. / Control of myeloid activity during retinal inflammation. In: Journal of Leukocyte Biology. 2003 ; Vol. 74, No. 2. pp. 161-166.
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AB - 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.

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