December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Modulation of Lymphocyte Activation by RPE Cells
Author Affiliations & Notes
  • KL Lew
    Ophthalmology University of Minnesota Minneapolis MN
  • SW McPherson
    Ophthalmology University of Minnesota Minneapolis MN
  • DS Gregerson
    Ophthalmology University of Minnesota Minneapolis MN
  • Footnotes
    Commercial Relationships   K.L. Lew, None; S.W. McPherson, None; D.S. Gregerson, None. Grant Identification: Support: NIH grant EY13249, RPB, MN Lions, and Anna Heilmaier Fund
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2286. doi:
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      KL Lew, SW McPherson, DS Gregerson; Modulation of Lymphocyte Activation by RPE Cells . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2286.

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

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Abstract: : Purpose:Studies of ocular immune privilege increasingly reveal a complex group of mechanisms that contribute to the privileged state. The retinal pigment epithelium (RPE), as part of the blood-retinal barrier, has been the subject of several reports which have found evidence for immunosuppressive properties. These include inhibition of lymphocyte proliferation experiments, and evidence that TGF-beta participates in this activity. We have also looked at the immunoregulatory properties of RPE cells in vitro. Our focus has been on activities that inhibit activation of NFAT-dependent cytokine production since this would lead to loss of proliferative responses. Methods:A Jurkat cell line was transfected with a secreted form of placental alkaline phosphatase regulated by the NFAT promoter. This promoter leads to high levels of alkaline phosphatase production when the Jurkat cells are stimulated through their T cell receptor using the C305 monoclonal antibody. RPE cells and their supernatants were tested for effects on Jurkat cell activation by measuring the output of this reporter. Lymphocyte proliferation assays, both antigen- and mitogen-driven, were also used. Results:RPE cells produce a supernatant factor that inhibits lymphocyte proliferation assays. This activity titrates and is heat-stable. A significant part of this activity appears to be TGF-beta. The RPE cells and supernatant were also tested for the ability to inhibit production of the NFAT reporter. RPE supernatant, whether applied as culture supe, or in a split well, had no inhibitory effect on the reporter. Instead, there was an increase in reporter production. The increase in the reporter was independent of stimulation of the Jurkat T cell receptor. Culture of the Jurkat cells in direct contact with the RPE did lead to a modest (35%) decrease in overall reporter levels following stimulation. However, there was still an increase in reporter if the C305 stimulation of the Jurkat cells was omitted. Conclusion:The interesting observation is that RPE produces a cell-free activity that stimulates the NFAT promoter of Jurkat cells. Since NFAT activation is the result of an increase in intracellular calcium, the results suggests that RPE cells produce a calcium response in the Jurkat cells. Other studies have shown that increases in T lymphocyte intracellular calcium, in the absence of costimulatory signals, is a pathway to anergy and/or apoptosis. This may provide evidence of another means by which RPE cells can regulate immune responses.

Keywords: 567 retinal pigment epithelium • 433 immune tolerance/privilege • 435 immunomodulation/immunoregulation 

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