November 1994
Volume 35, Issue 12
Free
Articles  |   November 1994
Human leukocyte antigen-class II-positive human corneal epithelial cells activate allogeneic T cells.
Author Affiliations
  • M Iwata
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania.
  • A Yagihashi
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania.
  • M I Roat
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania.
  • A Zeevi
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania.
  • Y Iwaki
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania.
  • R A Thoft
    Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania.
Investigative Ophthalmology & Visual Science November 1994, Vol.35, 3991-4000. doi:
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    • Get Citation

      M Iwata, A Yagihashi, M I Roat, A Zeevi, Y Iwaki, R A Thoft; Human leukocyte antigen-class II-positive human corneal epithelial cells activate allogeneic T cells.. Invest. Ophthalmol. Vis. Sci. 1994;35(12):3991-4000.

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

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Abstract

PURPOSE: To achieve a better understanding of the mechanism of corneal immune diseases, including corneal allograft rejection, the authors examined the potential of human corneal epithelial (HCE) cells to activate allogeneic T lymphocytes. METHODS: The mixed lymphocyte-HCE cell reaction (MLCER) was performed as follows: HCE cells from primary cultures, with or without treatment with interferon-gamma (IFN-gamma), were treated with mitomycin C and then mixed with peripheral blood lymphocytes (PBL) from normal volunteers. Triplicate cultures were incubated for 7 days. Interleukin-1-alpha (IL-1-alpha) was added to some cultures to examine its effect on MLCER: The lymphocyte responses were measured by 3H-thymidine uptake for the last 18 hours of incubation in MLCER: RESULTS: IFN-gamma-treated, HLA-class-II-bearing HCE cells stimulated allogenic lymphocytes, whereas IFN-gamma nontreated, class-II-negative HCE cells did not. The stimulation by IFN-gamma-treated HCE cells was blocked by anti-HLA class II monoclonal antibody. In addition, exogenous IL-1-alpha reduced the lymphocyte response in MLCER: This effort was inhibited by indomethacin. CONCLUSIONS: This study demonstrates that HLA-class-II-bearing HCE cells can activate allogeneic PBL by a major histocompatibility complex class II-dependent mechanism. In addition, HCE cells may regulate immune reactions, probably through prostaglandin production caused by IL-1.

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