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Tumor-specific Up-Regulation of the Nonclassical Class I HLA-G Antigen Expression in Renal Carcinoma¹

CEA, Service de Recherches en Hémato-Immunologie, DSV/DRM, Hôpital Saint-Louis, Centre Hayem, 75010 Paris [E. C. I., E. D. C., P. P.]; Unité INSERM U487, Institut Gustave Roussy, PR1, 94805 Villejuif [N. G., S. C., A. C.]; Département d’Anatomopathologie, Institut Gustave Roussy, 94805 Villejuif [M-J. T. L.]; and Unité d’Immunologie, Laboratoire de Suivi Biologique des Nouvelles Thérapies, Institut Gustave Roussy, 94805 Villejuif, [E. A.], France

HLA-G is a nonclassical class I antigen mainly expressed at the maternofetal interface during pregnancy where it is thought to downmodulate maternal immune response against the semiallogeneic fetus. Recent studies indicate that ectopic up-regulation of HLA-G expression on melanoma cells may also favor their escape from antitumor immune response. HLA-G expression was here investigated on paraffin-embedded tumor and adjacent normal renal tissues of 18 renal cell carcinoma (RCC) patients. We provide evidence that HLA-G antigen is differentially expressed in carcinoma and normal renal cells and that up-regulation of this antigen in the tumor cells is more frequent than alterations of other MHC class I or class II antigens. We also demonstrated that HLA-G cell surface expression and secretion is maintained in a tumor cell line (DM) established from an HLA-G-positive RCC lesion. Furthermore, we show that type I ( and ß) and, in particular, type II () IFN treatment enhances steady-state mRNA levels and cell surface expression of HLA-G in the DM cell line. As several studies suggest that HLA-G displays various functional features that allow down-modulation of immune response in vitro, we propose that selective in vivo expression of HLA-G may participate in the impairment of antitumor immunity in RCC.

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