| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
*
Department of Immune Regulation, Tokyo Medical and Dental University, Graduate School, Tokyo, Japan;
Department of Immunology, Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan;
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan; and
Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan
¶
Department of Immune Regulation, Tokyo Medical and Dental University, Graduate School, Tokyo, Japan;
||
Department of Immunology, Tokyo Metropolitan Organization for Medical Research, The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan;
#
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan;
**
Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan
Inhibitory receptors expressed on NK cells recognize MHC class I molecules and transduce negative signals to prevent the lysis of healthy autologous cells. The lectin-like CD94/NKG2 heterodimer has been studied extensively as a human inhibitory receptor. In contrast, in mice, another lectin-like receptor, Ly-49, was the only known inhibitory receptor until the recent discovery of CD94/NKG2 homologues in mice. Here we describe the expression and function of mouse CD94 analyzed by a newly established mAb. CD94 was detected on essentially all NK and NK T cells as well as small fractions of T cells in all mouse strains tested. Two distinct populations were identified among NK and NK T cells, CD94bright and CD94dull cells, independent of Ly-49 expression. The anti-CD94 mAb completely abrogated the inhibition of target killing mediated by NK recognition of Qa-1/Qdm peptide on target cells. Importantly, CD94bright but not CD94dull cells were found to be functional in the Qa-1/Qdm-mediated inhibition. In the presence of the mAb, activated NK cells showed substantial cytotoxicity against autologous target cells as well as enhanced cytotoxicity against allogeneic and "missing self" target cells. These results suggest that mouse CD94 participates in the protection of self cells from NK cytotoxicity through the Qa-1 recognition, independent of inhibitory receptors for classical MHC class I such as Ly-49.
This article has been cited by other articles:
|
|
 |
|
  P. Colmenero, A. L. Zhang, T. Qian, L. Lu, H. Cantor, K. Soderstrom, and E. G. Engleman Qa-1b-Dependent Modulation of Dendritic Cell and NK Cell Cross-Talk In Vivo J. Immunol., October 1, 2007; 179(7): 4608 - 4615. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Iizuka, T. Kaifu, A. Nakamura, M. Obinata, and T. Takai Establishment and Functional Characterization of Novel Natural Killer Cell Lines Derived from a Temperature-Sensitive SV40 Large T Antigen Transgenic Mouse J. Biochem., August 1, 2006; 140(2): 255 - 265. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Shirak, A. Bendersky, G. Hulata, M. Ron, and R. R. Avtalion Altered Self-Erythrocyte Recognition and Destruction in an Inbred Line of Tilapia (Oreochromis aureus) J. Immunol., January 1, 2006; 176(1): 390 - 394. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. A. Rabinovich, J. Li, R. Hurren, and R. G. Miller Immunosynapse formation coincides with rapid activation of NK cells by syngeneic T cells and correlates with clustering of MHC class I Int. Immunol., June 1, 2005; 17(6): 671 - 676. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Shimizu, J. Koike, H. Wakao, K.-i. Seino, H. Koseki, T. Kakiuchi, T. Nakayama, and M. Taniguchi Role of a NK receptor, KLRE-1, in bone marrow allograft rejection: analysis with KLRE-1-deficient mice Blood, August 1, 2004; 104(3): 781 - 783. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Toyama-Sorimachi, Y. Tsujimura, M. Maruya, A. Onoda, T. Kubota, S. Koyasu, K. Inaba, and H. Karasuyama Ly49Q, a member of the Ly49 family that is selectively expressed on myeloid lineage cells and involved in regulation of cytoskeletal architecture PNAS, January 27, 2004; 101(4): 1016 - 1021. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Koike, H. Wakao, Y. Ishizuka, T.-a. Sato, M. Hamaoki, K.-i. Seino, H. Koseki, T. Nakayama, and M. Taniguchi Bone Marrow Allograft Rejection Mediated by a Novel Murine NK Receptor, NKG2I J. Exp. Med., January 5, 2004; 199(1): 137 - 144. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. T. Wilhelm, J.-R. Landry, F. Takei, and D. L. Mager Transcriptional Control of Murine CD94 Gene: Differential Usage of Dual Promoters by Lymphoid Cell Types J. Immunol., October 15, 2003; 171(8): 4219 - 4226. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Tajima, T. Tanaka, T. Ebata, K. Takeda, A. Kawasaki, J. M. Kelly, P. K. Darcy, R. E. Vance, D. H. Raulet, K. Kinoshita, et al. Blastocyst MHC, a Putative Murine Homologue of HLA-G, Protects TAP-Deficient Tumor Cells from Natural Killer Cell-Mediated Rejection In Vivo J. Immunol., August 15, 2003; 171(4): 1715 - 1721. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Van Beneden, A. De Creus, F. Stevenaert, V. Debacker, J. Plum, and G. Leclercq Expression of Inhibitory Receptors Ly49E and CD94/NKG2 on Fetal Thymic and Adult Epidermal TCR V{gamma}3 Lymphocytes J. Immunol., April 1, 2002; 168(7): 3295 - 3302. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
