April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Complement Component C5a Induced Expression of Il-22 and Il-17 is Associated With Age-Related Macular Degeneration Pathogenesis
Author Affiliations & Notes
  • B. Liu
    Lab Immunology,
    National Eye Institute/NIH, Bethesda, Maryland
  • L. Wei
    Lab Immunology,
    National Eye Institute/NIH, Bethesda, Maryland
  • C. Meyerle
    DBE/CTB,
    National Eye Institute/NIH, Bethesda, Maryland
  • N. Sen
    Lab Immunology,
    National Eye Institute/NIH, Bethesda, Maryland
  • F. Forooghian
    Lab Immunology,
    National Eye Institute/NIH, Bethesda, Maryland
  • S. Chakrabarty
    Lab Immunology,
    National Eye Institute/NIH, Bethesda, Maryland
  • E. Y. Chew
    Epidemiology & Clinical Applications, National Eye Inst/NIH, Bethesda, Maryland
  • R. B. Nussenblatt
    Lab Immunology,
    National Eye Institute/NIH, Bethesda, Maryland
  • Footnotes
    Commercial Relationships  B. Liu, None; L. Wei, None; C. Meyerle, None; N. Sen, None; F. Forooghian, None; S. Chakrabarty, None; E.Y. Chew, None; R.B. Nussenblatt, None.
  • Footnotes
    Support  NIH intramural research program
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 409. doi:
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      B. Liu, L. Wei, C. Meyerle, N. Sen, F. Forooghian, S. Chakrabarty, E. Y. Chew, R. B. Nussenblatt; Complement Component C5a Induced Expression of Il-22 and Il-17 is Associated With Age-Related Macular Degeneration Pathogenesis. Invest. Ophthalmol. Vis. Sci. 2010;51(13):409.

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

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Abstract

Purpose: : Genetic association studies have suggested that the dysregulation of the complement system might play a role in the development of age-related macular degeneration (AMD). The goal of this study is to investigate if the complement activation component, C5a, could affect the human aquired immune response and its implication in the pathogenesis of AMD.

Methods: : Human peripheral blood mononuclear cells (PBMCs) were isolated from the blood of exudative form of AMD patients using a Ficoll gradient centrifugation protocol. Microarray and real-time polymerase chain reactions were used to detect mRNA expression of cytokines. Intracellular staining and enzyme-linked immunosorbent assays were used to measure protein expression. Apoptotic cells were detected by staining of cells with the annexin-V and analyzed by a FACS Caliber flow cytometer.

Results: : C5a induced IL-22 and IL-17 expression from human CD4+ T cells. This effect is dependent on the interaction between T cells and monocytes, B7 expression on monocytes and IL-1β expression, but independent of IL-23. Moreover, we demonstrated that C5a protected human T cells from undergoing spontaneous apoptosis. Importantly, we observed a higher level of IL-22 in AMD patients’ serum as well as C5aR expression on CD4+ T cells. When compared with controls, IL-22 was present in the vitreous of AMD patient.

Conclusions: : IL-22 and IL-17 have emerged as an important subset of cytokines that are believed to be critical for local chronic inflammation and autoimmunity. Thus, our data suggest a potential mechanism underlying chronic inflammation and retinal degeneration commonly seen in AMD.

Keywords: age-related macular degeneration • inflammation • cytokines/chemokines 
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