April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Retinal Pericytes Are Immunosuppressive
Author Affiliations & Notes
  • Feng Lin
    Pathology, Case Westersn Reserve university, Cleveland, Ohio
  • Nader Sheibani
    Ophthalmology and Visual Sciences, Univ of Wisconsin-Madison, Madison, Wisconsin
  • Timothy S. Kern
    Department of Medicine, Case Western Reserve Univ, Cleveland, Ohio
  • Suber S. Huang
    Ophthalmology, Univ Hosp Case Med Ctr, Cleveland, Ohio
  • Zhidan Tu
    Pathology, Case Westersn Reserve university, Cleveland, Ohio
  • Footnotes
    Commercial Relationships  Feng Lin, None; Nader Sheibani, None; Timothy S. Kern, None; Suber S. Huang, None; Zhidan Tu, None
  • Footnotes
    Support  NIH Grant EY020956
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2580. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Feng Lin, Nader Sheibani, Timothy S. Kern, Suber S. Huang, Zhidan Tu; Retinal Pericytes Are Immunosuppressive. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2580.

      Download citation file:

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

  • Supplements

Purpose: : Accumulating evidence indicates that the chronic inflammation plays important roles in the pathogenesis of diabetic retinopathy, but how such inflammation is controlled in the retinal capillaries is not clear. Retinal pericytes are critical for retinal vascular integrity which contributes to the blood-retina barrier to maintain the immunoprivileged status of the eye. The loss of the retinal pericytes is a hallmark of early stage diabetic retinopathy. We hypothesize that retinal pericytes are immunosuppressive, therefore the loss of them favors retinal inflammation. In this study, we investigated whether retinal pericytes inhibit immune responses.

Methods: : Retinal pericytes were isolated from transgenic Immortomice (C57BL/6 background) and characterized. The immunosuppressive potential of the pericytes was assessed by CFSE-based T and B cell proliferation assays. In brief, to determine whether retinal pericytes suppress T cell responses, CFSE-labeled T cells were activated by antigen presenting cells together with anti-CD3 mAbs, and then co-cultured with different numbers of retinal pericytes. After incubation, the T cell proliferation was assessed by measuring CFSE fluorescence dilution using flow cytometry. To determine whether pericytes suppress B cell responses, CFSE-labeled B cells were activated by anti-CD40and IL-4, then co-cultured with different numbers of pericytes. After incubation, the B cell proliferation was assessed by flow cytometry similarly to that in the T cell assays. To determine whether soluble factors and/or cell-cell contact are required for inhibiting T and B cell responses, retinal pericytes cultured in a transwell system were investigated using the same methods described above.

Results: : Retinal pericytes are highly immunosuppressive. The isolated retinal pericytes potently inhibit both T and B cell proliferation in a dose-dependent manner. The T and B cell inhibitory activity of retinal pericytes decreases but does not abolish in transwell experiments, indicating that both soluble factors and cell-cell contact are involved in the retinal pericyte-mediated immunosuppression.

Conclusions: : These results reveal a new function of retinal pericytes, suggesting that the immunosuppressive activity of the retinal pericytes contributes to ocular immune privilege. This also offers a novel mechanism by which pericyte loss might contribute to the development of diabetic retinopathy.

Keywords: diabetic retinopathy • immune tolerance/privilege • immunomodulation/immunoregulation 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.