September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Inflammatory cytokines primes retinal pigment epithelial cells to complement activation and deposition of membrane attack complexes by the alternative pathway
Author Affiliations & Notes
  • Carsten Faber
    Department of Immunology and Microbiology, University of Copenhagen, Faculty of Health and Medical Sciences, Copenhagen N, Denmark
    Department of Ophthalmology, Copenhagen University Hospital, Rigshospitalet - Glostrup, Glostrup, Denmark
  • Christian Tagmose
    Department of Immunology and Microbiology, University of Copenhagen, Faculty of Health and Medical Sciences, Copenhagen N, Denmark
  • Peter Garred
    Department of Clinical Immunology, Laboratory of Molecular Medicine, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
  • Mogens Holst Nissen
    Department of Immunology and Microbiology, University of Copenhagen, Faculty of Health and Medical Sciences, Copenhagen N, Denmark
  • Footnotes
    Commercial Relationships   Carsten Faber, None; Christian Tagmose, None; Peter Garred, None; Mogens Holst Nissen, None
  • Footnotes
    Support  Fight for Sight Denmark
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 475. doi:
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    • Get Citation

      Carsten Faber, Christian Tagmose, Peter Garred, Mogens Holst Nissen; Inflammatory cytokines primes retinal pigment epithelial cells to complement activation and deposition of membrane attack complexes by the alternative pathway. Invest. Ophthalmol. Vis. Sci. 2016;57(12):475.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : To examine how inflammatory cytokines influence the interaction between retinal pigment epithelial (RPE) cells and the complement system in relation to age-related macular degeneration (AMD).

Methods : Post-confluent ARPE-19 were cultivated in serum-free conditions, exposed to inflammatory stimulation by CD3/CD28 stimulated PBMC or interferon gamma (IFNγ) and tumor necrosis factor alpha (TNFα) for 48 hours. After multiple washes, the primed ARPE-19 were exposed to diluted serum from healthy donors or complement factor B (CFB)-deficient serum. Anti-C5 was added in some experiments. Deposition of membrane attack complexes (MAC) was examined by modified use of a MAC-ELISA kit and by immunofluorescence.

Results : MAC was deposited on ARPE-19 exposed to either stimulated PBMC or IFNγ and TNFα. MAC was not deposited on unstimulated ARPE-19. Lack of complement factor B or inhibition of C5 also abrogated the MAC-deposition, while reconstitution of deficient serum with CFB resulted in MAC-deposition.

Conclusions : Inflammatory stimulation of ARPE-19 promoted alternative pathway activation of complement and deposition of MAC. These results suggests that circulating inflammatory mediators may increase susceptibility to local complement activation and MAC-deposition on RPE.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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