Evidence that the cellular ligand for the human NK cell activation receptor NKp30 is not a heparan sulfate glycosaminoglycan
JOURNAL OF IMMUNOLOGY
Authors: Warren, HS; Jones, AL; Freeman, C; Bettadapura, J; Parish, CR
Abstract
NKp30 (NCR3, CD337) is a natural cytotoxicity receptor, expressed on subsets of human peripheral blood NK cells, involved in NK cell killing of tumor cells and immature dendritic cells. The cellular ligand for NKp30 has remained elusive, although evidence that membrane-associated heparan sulfate (HS) proteoglycans are involved in the recognition of cellular targets by NKp30 was recently reported. The data presented in this report show conclusively that HS glycosaminoglycans (GAG) are not ligands for NKp30. We show that removing HS completely from the cell surface of human 293-EBNA cells with mammalian heparanase does not affect binding of rNKp30/human IgG1 Fc chimera complexes or binding of multimeric liposome-rNKp30 complexes. Removing HS from 293-EBNA cells, culture-generated DC, MM-170 malignant melanoma cells, or HeLa cells does not affect the NKp30-dependent killing of these cells by NK cells. We show further that the GAG-deficient hamster pgsA-745 cells that lack HS and the GAG-expressing parent CHO-K1 cells are both killed by NK cells, with killing of both cell lines inhibited to the same extent by anti-NKp30 mAb. From these results we conclude that HS GAG are not ligands for NKp30, leaving open the question as to the nature of the cellular ligand for this important NK cell activation receptor.
Hydrazo-keto and azo-enol tautomerism in organometallic palladacycles. New bidentate monoanionic and tridentate bianionic ligands
JOURNAL OF THE CHEMICAL SOCIETY-DALTON TRANSACTIONS
Authors: Albert, J; Gonzalez, A; Granell, J; Moragas, R; Solans, X; Font-Bardia, M
Abstract
The action of PdCl2 on phenylhydrazones derived from 2-oxopropionaldehyde, benzoylformaldehyde or butane-2,3-dione led to dinuclear metallacycles 1 [{Pd[2-((NRN)-N-4=(CRCRO)-C-3-O-2)-5-(RC6H3)-C-1]Cl}(2)] (R-1 = H, Pr, NO2 or MeO; R-2 = Me or Ph; R-3, R-4 = H or Me). Compounds 1 reacted with PPh3 to afford [PdCl{kappa C,kappa N-(C-N)} (PPh3)] 2 or [PdCl{kappa C-(C-N)}(PPh3)(2)] 3 (C-N being the metallated hydrazone) which contain one or two phosphine molecules per metal atom respectively, depending on the steric hindrance of the N-donor ligands. The structure of [Pd{2-(NHN=CHCOMe)-5 -O2NC6H3} Cl(PPh3)] has been determined by X-ray diffraction. The bond distances and angles are similar to those reported for related metallacycles. The distance N(1)...O(1) [2.631(4) Angstrom] indicates the presence of a strong intramolecular hydrogen bond between the NH and COMe groups. The C(8)-O(1) [1.222(5) Angstrom], C(8)-C(7)[1.470(5) Angstrom], C(7)-N(2) [1.304(4) Angstrom] and N(1)-N(2) [1.342(4) Angstrom] bond lengths indicate that the complex 3 exists mainly in the keto-hydrazo form. The action of NaOMe on the PPh3 or (PPh3)(2) complexes in MeOH afforded deep violet compounds which do not contain chlorine atoms. The analytical data, IR and NMR spectra showed that deprotonation of the NH group had taken place to give[Pd {2-(N=NCR3=(CRO)-O-2)-5-(RC6H3)-C-1}(PPh3)], by means of an hydrazo-keto azo-enol tautomerization.