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Blood, 1 August 2005, Vol. 106, No. 3, pp. 956-962. Prepublished online as a Blood First Edition Paper on April 12, 2005; DOI 10.1182/blood-2004-10-4159. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-4159v1 106/3/956    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Stevenaert, F. Articles by Leclercq, G. Search for Related Content PubMed PubMed Citation Articles by Stevenaert, F. Articles by Leclercq, G. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Ly49 and CD94/NKG2 receptor acquisition by NK cells does not require lymphotoxin- receptor expression Frederik Stevenaert, Katrien Van Beneden, Veerle De Colvenaer, Ann Sophie Franki, Veronique Debacker, Tom Boterberg, Dieter Deforce, Klaus Pfeffer, Jean Plum, Dirk Elewaut, and Georges Leclercq From the Department of Clinical Chemistry, Microbiology, and Immunology, Ghent University, Ghent, Belgium; the Rheumatology Division, Department of Internal Medicine, Ghent University, Ghent, Belgium; the Department of Pharmaceutical Biotechnology, Ghent University, Ghent, Belgium; the Department of Radiotherapy, Ghent University, Ghent, Belgium; and the Institute of Medical Microbiology, University of Dusseldorf, Dusseldorf, Germany. A crucial step in murine natural killer (NK) cell development, mediated by bone marrow stromal cells, is the induction of Ly49 and CD94/NKG2 receptor expression. The signals that regulate Ly49 receptor expression are still largely undetermined. It has been shown that interaction between lymphotoxin 12 (LT12) and LT receptor (LTR), expressed on lymphoid progenitor cells and nonlymphoid bone marrow stromal cells, respectively, is important for both quantitative and functional NK cell development. Therefore, we have investigated the role of LT-LTR–mediated signaling in Ly49 and CD94/NKG2 receptor acquisition. We show that the NK receptor repertoire of LTR–/– mice can only be partially analyzed because of the residual 129/Ola mouse genetic background, due to a physical linkage of the LTR locus and the loci encoding the Ly49 and CD94/NKG2 receptors. Therefore, we transferred wild-type B6 lymphoid-committed progenitor cells into LTR–/– mice, which differentiated into NK cells with a normal NK cell receptor repertoire. Also, administration of LTR-immunoglobulin (Ig), which acts as a soluble receptor for LT12, resulted in reduced NK cell percentages but did not influence the Ly49 and CD94/NKG2 receptor acquisition on remaining NK cells. These results indicate that LTR-mediated signals are not required for Ly49 and CD94/NKG2 receptor acquisition. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Kim, A. Saudemont, L. Webb, M. Camps, T. Ruckle, E. Hirsch, M. Turner, and F. Colucci The p110delta catalytic isoform of PI3K is a key player in NK-cell development and cytokine secretion Blood, November 1, 2007; 110(9): 3202 - 3208. [Abstract] [Full Text] [PDF]

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