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The Journal of Immunology, 1999, 162: 5902-5909.
Copyright © 1999 by The American Association of Immunologists

Trophoblast Cell Line Resistance to NK Lysis Mainly Involves an HLA Class I-Independent Mechanism1

Tony Avril2,*, Annie-Claude Jarousseau2,*, Herve Watier*, Jose Boucraut{dagger}, Philippe Le Bouteiller{ddagger}, Pierre Bardos* and Gilles Thibault3,*

* UPRES-JE 1992 Interactions Hôte-Greffon, Laboratoire d’Immunologie, Faculté de Médecine, Tours, France; {dagger} Laboratoire d’Immunologie, Faculté de Médecine de la Timone, Marseille, France; and {ddagger} Institut National de la Santé et de la Recherche Médicale, U395, CHU Purpan, Toulouse, France

The lack of classical HLA molecules on trophoblast prevents allorecognition by maternal T lymphocytes, but poses the problem of susceptibility to NK lysis. Expression of the nonclassical class I molecule, HLA-G, on cytotrophoblast may provide the protective effect. However, the class I-negative syncytiotrophoblast escapes NK lysis by maternal PBL. In addition, while HLA-G-expressing transfectants of LCL.721.221 cells are protected from lymphokine-activated killer lysis, extravillous cytotrophoblast cells and HLA-G-expressing choriocarcinoma cells (CC) are not. The aim of this work was therefore to clarify the role of HLA class I expression on trophoblast cell resistance to NK lysis and on their susceptibility to lymphokine-activated killer lysis. Our results showed that both JAR (HLA class I-negative) and JEG-3 (HLA-G- and HLA-Cw4-positive) cells were resistant to NK lysis by PBL and were equally lysed by IL-2-stimulated PBL isolated from a given donor. In agreement, down-regulating HLA class I expression on JEG-3 cells by acid treatment, masking these molecules or the putative HLA-G (or HLA-E) receptor CD94/NKG2 and the CD158a/p58.1 NKR with mAbs, and inducing self class I molecule expression on JAR cells did not affect NK or LAK lysis of CC. These results demonstrate that the resistance of CC to NK lysis mainly involves an HLA class I-independent mechanism(s). In addition, we show that the expression of a classical class I target molecule (HLA-B7) on JAR cells is insufficient to induce lysis by allospecific polyclonal CTL.




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