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HLA-G Proteins in Cancer: Do They Provide Tumor Cells with an Escape Mechanism?

¹ Service de Recherche en Hémato-Immunologie, Direction des Sciences du Vivant, Département de Recherche Médicale, Commissariat à l'Energie Atomique, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France and ² Department of Immunology, Roswell Park Cancer Institute, Buffalo, New York

Requests for reprints: Edgardo D. Carosella, Service de Recherche en Hémato-Immunologie, Direction des Sciences du Vivant, Département de Recherche Médicale, Commissariat à l'Energie Atomique, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, avenue Claude Vellefaux, 75475 Paris cedex 10, France. Phone: 33-1-53-72-22-27; Fax: 33-1-48-03-19-60; E-mail: carosella{at}dsvidF.cea.Fr.

Abstract

Convincing clinical evidence indicates that the limited success of T-cell–based immunotherapy of malignant diseases is caused, at least in part, by the ability of malignant cells to escape from immune recognition and destruction. Among the multiple escape mechanisms identified, a major role is played by changes in the expression and/or function of HLA antigens expressed by tumor cells, because they may markedly affect tumor cell-host's immune system interactions. In this article, we review the data about the aberrant expression of the nonclassical HLA class I antigen HLA-G by tumor cells. Furthermore, we discuss the possible reasons for the conflicting information in the literature about HLA-G antigen expression by malignant cells. Lastly, in light of the well-documented immunotolerant function of HLA-G, we discuss the potential role of these antigens in the escape of tumor cells from immune recognition and destruction and in the clinical course of malignant diseases.

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