| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Etablissement Français du Sang, Université de Nantes, ImmunoVirologie et Polymorphisme Génétique, EA4271, Nantes, France;
Laboratoire d’Histocompatibilité, Etablissement Français du Sang, Nantes, France; and
Université de Nantes, Biostatistique, Recherche Clinique et Mesures Subjectives en Santé, EA4275, Faculté de Pharmacie, Nantes, France
Recently, the Z27 mAb was shown to recognize the NK cell-activating receptor KIR3DS1, and several genetic studies suggest that the most probable ligands of KIR3DS1 are HLA class I molecules with the Bw4 motif. Despite these findings, the attempts to establish a functional interaction between KIR3DS1 and its potential ligand have been unsuccessful. Here, we study the proliferation and cytotoxicity of KIR3DS1+ NK cells, compared with KIR3DL1+ NK cells, according to the Bw4+ or Bw4– allogeneic environment. Our results show for the first time that KIR3DS1 expression on NK cells can be induced after exposure to stimulator cells (221, K562, EBV-B cell lines, and B cells), polyinosinic-polycytidylic acid, IL-15, or IL-2. Furthermore, whereas KIR3DL1+ NK cell proliferation and cytotoxicity were inhibited in a Bw4+ but not a Bw4– context, KIR3DS1+ NK cell functions were not influenced by the presence of Bw4 on target cells. Nevertheless, despite the absence of demonstrated regulation of KIR3DS1+ NK cell functions by HLA-Bw4 molecules, we found a higher KIR3DS1+ NK cell frequency and higher levels of KIR3DS1 expression in Bw4+ compared with Bw4– individuals. Altogether, these results suggest that KIR3DS1 does not recognize HLA-Bw4 molecules in a physiological context, and they highlight the induced expression of KIR3DS1 observed on stimulated NK cells and the higher frequency of KIR3DS1+ NK cells in Bw4+ individuals. Because a protective KIR3DS1-Bw4 association has been reported in viral infections, our results further the understanding of the role of KIR3DS1+ NK cells in controlling viral infections.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by Etablissement Français du Sang, Université de Nantes, Ligue contre le Cancer, and Nantes Atlantique Greffe de Moelle Osseuse association. M.M. is a Ph.D. candidate supported by Comité Départemental de Loire-Atlantique de la Ligue contre le Cancer.
2 Address correspondence and reprint requests to Dr. Christelle Retière, EA4271 ImmunoVirologie et Polymorphisme Génétique, Etablissement Français du Sang, 34 Boulevard Jean Monnet, Nantes, F-44011 Cedex, France. E-mail address: christelle.retiere{at}efs.sante.fr
3 Abbreviations used in this paper: KIR, killer-Ig like receptor; MFI, mean channel fluorescence intensity; poly(IC), polyinosinic-polycytidylic acid.
4 The online version of this article contains supplemental material.
This article has been cited by other articles:
|
|
 |
|
  D. Sharma, K. Bastard, L. A. Guethlein, P. J. Norman, N. Yawata, M. Yawata, M. Pando, H. Thananchai, T. Dong, S. Rowland-Jones, et al. Dimorphic Motifs in D0 and D1+D2 Domains of Killer Cell Ig-Like Receptor 3DL1 Combine to Form Receptors with High, Moderate, and No Avidity for the Complex of a Peptide Derived from HIV and HLA-A*2402 J. Immunol., October 1, 2009; 183(7): 4569 - 4582. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
