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An Epithelial Cell Line That Can Stimulate Alloproliferation of Resting CD4⁺ T Cells, But Not After IFN- Stimulation¹

Charlotte Lawson^*, Ann M. McCormack^*, David Moyes^*, Sheng Yun, John W. Fabre, Magdi Yacoub^* and Marlene L. Rose^2,*

^* Transplant Immunology Group, Imperial College School of Medicine, National Heart and Lung Institute, Heart Science Centre, Harefield Hospital, Harefield, Middlesex, United Kingdom; and Department of Clinical Sciences, Institute of Liver Studies, Kings College Hospital, London, United Kingdom

It has previously been shown that IFN--induced up-regulation of HLA class II on the surface of epithelial cells is not sufficient to induce proliferation of allospecific CD4⁺ T cells in vitro. To further investigate this phenomenon, a human epithelial bladder carcinoma, T24, was induced to constitutively express HLA class II without IFN- stimulation, by permanent transfection with the full-length class II transactivator (CIITA) gene. Proliferation of allospecific T cells to transfected and wild-type cells with and without prior activation with saturating levels of IFN- for 4 days was examined. IFN--activated T24 did not induce any response from CD4⁺ T cells. However, T24.CIITA induced significant levels of alloproliferation, which could be abrogated by pretreatment of T24.CIITA with a mAb to LFA-3. Prestimulation of T24.CIITA with saturating levels of IFN- for 4 days also prevented allospecific CD4⁺ T cell proliferation. These findings suggest that epithelial cells may be intrinsically able to process and present alloantigen and provide adequate costimulation. We propose that IFN- has a secondary, as yet unidentified, effect that acts to negatively regulate this response, at least in some epithelial cells.

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				S. S. Tay, A. McCormack, C. Lawson, and M. L. Rose IFN-{gamma} Reverses the Stop Signal Allowing Migration of Antigen-Specific T Cells into Inflammatory Sites J. Immunol., March 15, 2003; 170(6): 3315 - 3322. [Abstract] [Full Text] [PDF]