Identification of murine natural killer cell subsets with monoclonal antibodies derived from 129 anti-C57BL/6 immune spleen cells

Lemieux, Suzanne; Ouellet-Talbot, F; Lusignan, Y; Morelli, Lidia; Labrèche, N; Gosselin, Pierre; Lecomte, Jacqueline

doi:10.1016/0008-8749(91)90342-9

Cited by 16 publications

(7 citation statements)

References 30 publications

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“…The following antibodies were obtained from BD Biosciences: APC-PK136 (anti-NK1.1), PerCP-Cy5.5-145-2C11 (anti-CD3) and PerCP-Cy5.5-1D3 (anti-CD19), and FITC-M1/70 (anti-CD11b) and FITC-S7 (anti-CD43). Biotinylated-3D10 (anti-Ly49H) ( 6 ), FITC-4E4 (anti-Ly49D) ( 52 ), 4LO3311 (anti-Ly49C) ( 53 ), and FITC-JR9 (anti-Ly49A) ( 6 ) were purifi ed from hybridomas and conjugated to FITC using FITC-celite (Calbiochem) or biotin using EZ-Link Sulfo-NHS-LC-LC-Biotin (Thermo Fisher Scientifi c) according to manufacturer ' s protocol. Digoxigenin labeling of anti-Ly49C was performed according to manufacturer ' s protocol using the DIG Protein Labeling kit (Roche).…”

Section: Methodsmentioning

confidence: 99%

Continuous engagement of a self-specific activation receptor induces NK cell tolerance

Tripathy¹,

Keyel

Yang

et al. 2008

The Journal of Experimental Medicine

150

151

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Abbreviations used: LAK, lymphokine-activated killer; m157-Tg, m157 transgenic; MCMV, murine cytomegalovirus; poly I: C, polyinosinic:polycytidylic acid.The online version of this article contains supplemental material. Natural killer (NK) cell tolerance mechanisms are incompletely understood. One possibility is that they possess self-specifi c activation receptors that result in hyporesponsiveness unless modulated by self -major histocompatability complex (MHC) -specifi c inhibitory receptors. As putative self-specifi c activation receptors have not been well characterized, we studied a transgenic C57BL/6 mouse that ubiquitously expresses m157 (m157-Tg), which is the murine cytomegalovirus (MCMV) -encoded ligand for the Ly49H NK cell activation receptor. The transgenic mice were more susceptible to MCMV infection and were unable to reject m157-Tg bone marrow, suggesting defects in Ly49H + NK cells. There was a reversible hyporesponsiveness of Ly49H + NK cells that extended to Ly49H-independent stimuli. Continuous Ly49H -m157 interaction was necessary for the functional defects. Interestingly, functional defects occurred when mature wild-type NK cells were adoptively transferred to m157-Tg mice, suggesting that mature NK cells may acquire hyporesponsiveness. Importantly, NK cell tolerance caused by Ly49H -m157 interaction was similar in NK cells regardless of expression of Ly49C, an inhibitory receptor specifi c for a self-MHC allele in C57BL/6 mice. Thus, engagement of self-specifi c activation receptors in vivo induces an NK cell tolerance effect that is not affected by self-MHC -specifi c inhibitory receptors.

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Section: Methodsmentioning

confidence: 99%

Continuous engagement of a self-specific activation receptor induces NK cell tolerance

Tripathy¹,

Keyel

Yang

et al. 2008

The Journal of Experimental Medicine

150

151

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“…[10,17,18,29]. Through the generation of the 4LO3311 monoclonal antibody [30], direct analysis of the inhibitory receptor Ly49C, a receptor with implicated specificity for H-2K b [26][27][28], was made possible. NK1.1 + cells in wild-type, TAP1−/−, g 2m−/− and TAP1/ g 2m−/− mice all express similar numbers of Ly49C + cells (approximately 30 % of NK1.1 + cells in the spleen).…”

Section: Self Tolerance Of Nk Cells From Mhc Class Ideficient Mice Ismentioning

confidence: 99%

“…Anti-NK1.1 monoclonal antibodies (PK136) were purchased from Pharmingen (San Diego, CA). The Ly49C-specific monoclonal antibody (4LO3311) has been described [30]. To enrich for NK cells, erythrocyte-depleted spleen cells from individual mice were resuspended in RPMI medium supplemented with 10 % FCS (RPMI/10 % FCS) and loaded onto equilibrated nylon wool (Polyscience, Germany) columns that had been pre-incubated at 37°C for 45 min.…”

Section: Antibodies and Flow Cytometrymentioning

confidence: 99%

Fine tuning of natural killer cell specificity and maintenance of self tolerance in MHC class I-deficient mice

et al. 1998

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TAP1 −/−, β2‐microglobulin (β2m) −/− and TAP1/β2m −/− mice all express low but quantitatively different levels of MHC class I molecules. Using these mice, we have addressed questions relating to the fine tuning of natural killer (NK) cell specificity and maintenance of self tolerance in the NK cell system. NK cells from B6 wild‐type mice killed target cells from TAP1 −/−, β2m −/− and TAP1/β2m −/− mice in vivo and rejected bone marrow grafts from the same mice in vivo at equivalent levels. NK cells from TAP1 −/−, β2m −/− mice did not kill target cells or reject bone marrow grafts from TAP1/β2m −/− mice. NK cells in all MHC class I‐deficient mice were tolerant to autologous MHC class I‐deficient cells, as revealed by in vitro cytotoxicity assays using NK cell effectors activated with the interferon‐inducing agent Tilorone, or by in vivo bone marrow graft experiments. However, the self‐tolerant state of MHC class I‐deficient NK cells was broken by in vitro stimulation with IL‐2 for 4 days. Under these conditions, NK cells from the MHC class I‐deficient mice killed autologous MHC class I‐deficient cells while MHC class I‐positive targets were spared. The C‐type lectin inhibitory receptor Ly49C has a specificity for H‐2Kb and is expressed on a subset of NK1.1+ cells in B6 mice. Wild‐type and all MHC class I‐deficient mice had similar numbers of Ly49C‐positive NK1.1+ cells. However, Ly49C expression was markedly down‐regulated on NK1.1+ cells from B6 mice, as compared to TAP1 −/−, β2m −/− and TAP1/β2m −/− mice. In vitro stimulation of NK cells with IL‐2 for 4 days did not significantly change this pattern. The present results are discussed in relation to the role of MHC class I molecules and Ly49 receptors in shaping the NK cell repertoire and raise new questions about maintenance of self tolerance in the NK cell system.

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“…The Sundback cDNA sequence is hkely to represent the B6 allele of Ly49C; the other B6 sequence has been designated Ly491 by Takei and colleagues (34). As discussed by Takei and colleagues elsewhere in this volume, the products of both Ly491 and Ly49C bind 5E6 mAb, while the 4L033 11 mAb (also designated NK2.1) generated by Lemieux et al (35,36) recognizes only Ly49C (both B6 and BALB alleles) (34).…”

Section: Missing Self Hypothesismentioning

confidence: 99%

Allorecognition by murine natural killer cells: lysis of T‐lymphoblasts and rejection of bone‐marrow grafts

George

Liu

et al. 1997

Immunological Reviews

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Natural killer (NK) cells of inbred mice reject allogeneic bone-marrow cells, and NK cells of F1 hybrid mice can reject parental bone-marrow cells (hybrid resistance). In some cases these patterns of rejection can be mimicked in vitro by utilizing IL-2 cultured NK effector cells and allogeneic or parental T-lymphoblasts as target cells. Lysis of allogeneic and parental targets in vitro can be explained on the basis of the missing self hypothesis. Subsets of NK cells that bear non-overlapping MHC class I inhibitory receptors belonging to the Ly49 family lyse allogeneic targets because they do not express self class I molecules of the NK cell donor. Parental strain targets are lysed because they do not express all of the self class I antigens of the F1 hybrid, and hence fail to deliver inhibitory signals to all subsets of F1 NK cells. The expression of Ly49 receptors on NK cells is regulated by host MHC to ensure maximal sensitivity to alterations in self class I molecules and to prevent autoreactivity. In many instances, however, the rejection of allogeneic bone marrow cells in vivo cannot be readily explained by the missing self hypothesis. In these instances, it appears that rejection is initiated by class I MHC receptors on NK cells that recognize allogeneic class I molecules as non-self, and activate rather than inhibit NK cell function.

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Identification of murine natural killer cell subsets with monoclonal antibodies derived from 129 anti-C57BL/6 immune spleen cells

Cited by 16 publications

References 30 publications

Continuous engagement of a self-specific activation receptor induces NK cell tolerance

Continuous engagement of a self-specific activation receptor induces NK cell tolerance

Fine tuning of natural killer cell specificity and maintenance of self tolerance in MHC class I-deficient mice

Allorecognition by murine natural killer cells: lysis of T‐lymphoblasts and rejection of bone‐marrow grafts

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