Biol Reprod Lalor Postdoctoral Fellowships -- Application Deadline January 15, 2009
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

BOR - Papers in Press, published online ahead of print April 30, 2003.
Biol Reprod 2003, 10.1095/biolreprod.102.009290
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
69/2/627    most recent
biolreprod.102.009290v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Avril, T.
Right arrow Articles by Thibault, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Avril, T.
Right arrow Articles by Thibault, G.
Agricola
Right arrow Articles by Avril, T.
Right arrow Articles by Thibault, G.
BIOLOGY OF REPRODUCTION 69, 627–633 (2003)
DOI: 10.1095/biolreprod.102.009290
© 2003 by the Society for the Study of Reproduction, Inc.

Immunology

Human Choriocarcinoma Cell Resistance to Natural Killer Lysis Due to Defective Triggering of Natural Killer Cells1

Tony Avril3, Sophie Iochmann3, Denys Brand4, Pierre Bardos3, Hervé Watier3, and Gilles Thibault2,3

EA 3249 «Cellules hématopoïétiques, hémostase et greffe»3 EA 3250 «Microbiologie médicale et moléculaire»,4 Faculté de Médecine, Tours, France

The trophoblast, the outermost layer of the human placenta, lacks expression of the classical human leukocyte antigen (HLA) class I molecules. This prevents allorecognition by T cells but raises the question of what protects the trophoblast from natural killer (NK) cells. In a previous study, we have shown that choriocarcinoma cell (CC) resistance to NK lysis was mainly independent of HLA class I molecules. In the present study, we postulated that CC may prevent activation of NK cells by failing to stimulate their triggering receptors (TR). To test this hypothesis, we evaluated the lysis of JAR and JEG-3 CC after effective cross-linking and activation of NK cells by means of lectins or antibodies. Our results show that NK-resistant CC were sensitive to lysis by unstimulated peripheral blood lymphocytes in the presence of phytohemagglutin (PHA), to antibody-dependent cell cytotoxicity in presence of anti-Tja antibodies, and to monoclonal antibody redirected killing using anti-TR antibodies anti-CD16 and anti-CD244/2B4. Finally, CC fail to express CD48, the ligand for CD244/2B4. These results indicate that the resistance of CC to lysis results primarily from defective NK cell activation, at least partially due to the lack of expression of ligands, such as CD48, involved in the triggering of NK cells.

1 This work was supported by Fondation Langlois. T.A. was supported by a grant from the French Society of Transplantation.

2 Correspondence: G. Thibault, EA 3249 «Cellules hématopoïétiques, hémostase et greffe», Laboratoire d'Immunologie, Faculté de Médecine, 2 bis boulevard Tonnellé, 37032 Tours Cedex, France. FAX: 33 2 4736 6095; thibault{at}med.univ-tours.fr






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2003 by the Society for the Study of Reproduction.