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Soluble HLA-G Inhibits Cell Cycle Progression in Human Alloreactive T Lymphocytes¹

Rajia Bahri^*, Francois Hirsch^*, Adeline Josse^*, Nathalie Rouas-Freiss, Nicolas Bidere^*, Aime Vasquez^*, Edgardo D. Carosella, Bernard Charpentier^*, and Antoine Durrbach^2,*,

^* Institut National de la Santé et de la Recherche Médicale Unité 542, Villejuif, France; Service de Recherches en Hémato-Immunologie, Centre Energie Atomique, Hôpital Saint-Louis, University Hospital, Paris, France; and Département de Néphrologie, Hôpital du Kremlin-Bicêtre, Le Kremlin-Bicêtre, France

HLA-G is involved in regulating T cell responses. Various mechanisms have been proposed to explain the inhibition of T cell proliferation. In this context, the possible role of HLA-G in cell cycle regulation remains to be explored. Using stably transfected M8 cells expressing the secreted isoform (HLA-G5) of HLA-G, we investigated the role of HLA-G in inducing apoptosis and in controlling the cell cycle of activated T cells. Soluble HLA-G (HLA-G5) inhibited both CD4 and CD8 T cell proliferation. However, HLA-G5 did not induce T cell apoptosis, as determined by 3,3'-diethyloxacarbocyanine and propidium iodine labeling. It induced accumulation of the retinoblastoma protein, but not its phosphorylated and active form. Treatment of activated T cells with HLA-G5 also reduced the amounts of cyclin D2, E, A, and B by >80%. In contrast, it induced an accumulation of p27^kip, but not p21^cip, in activated T cells. HLA-G does not induce apoptosis of alloreactive T cells, but induces p27^kip1 and inhibits cell cycle progression.

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