Monoclonal antibody to a triggering structure expressed on rat natural killer cells and adherent lymphokine-activated killer cells.

Chambers, William H.; Vujanović, Nikola L.; DeLeo, Albert B.; Olszowy, Michael W.; Herberman, Ronald B.; Hiserodt, John C.

doi:10.1084/jem.169.4.1373

Cited by 346 publications

(189 citation statements)

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“…For flow cytometry, 1-10 Â 10 5 cells were labeled with different combinations of the following mAb: 3.2.3 (anti-NKR-P1A, anti-NKR-P1B F344 , [3]), STOK27 (anti-NKR-P1B PVG , [18]), or M2 (anti-FLAG; Sigma). Primary cells were enriched for mononuclear cells by centrifugation on Lymphoprep before use.…”

Section: Flow Cytometry Mab and Cellsmentioning

confidence: 99%

“…These are type II transmembrane proteins encoded by the NK gene complex (NKC), which is located on chromosome 4 in the rat [1,2]. The NKR-P1 molecules (KLRB or CD161) were among the first KLR to be characterized, but their function long remained elusive [3][4][5]. Although the NKR-P1 family has expanded to include both activating and inhibitory members in rodents, it consists of only one member in several other mammalian species, including in human [6].…”

Section: Introductionmentioning

confidence: 99%

“…In the rat, four full-length Nkrp1 genes are present in the BN strain genome, Nkrp1a, -b, -f, and -g. The NKR-P1A molecule reacts with mAb 3.2.3 (or 10/78), which is used as a prototypic NK-cell marker in the rat [3,4,15]. We have recently shown that mAb 3.2.3 (or 10/78) fails to stain NK cells from selected strains, analogous to the situation for the NK1.1 marker in mice [16].…”

Section: Introductionmentioning

confidence: 99%

“…In human, the NKR-P1A receptor binds a Clr orthologue termed lectin-like transcript 1(LLT1), which is able to specifically inhibit NK cytolytic activity and cytokine production [12][13][14]. In the rat, four full-length Nkrp1 genes are present in the BN strain genome, Nkrp1a, -b, -f, and -g. The NKR-P1A molecule reacts with mAb 3.2.3 (or 10/78), which is used as a prototypic NK-cell marker in the rat [3,4,15]. We have recently shown that mAb 3.2.3 (or 10/78) fails to stain NK cells from selected strains, analogous to the situation for the NK1.1 marker in mice [16].…”

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confidence: 99%

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Two major groups of rat NKR‐P1 receptors can be distinguished based on chromosomal localization, phylogenetic analysis and Clr ligand binding

et al. 2009

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A major subset of non-alloreactive NK cells in PVG strain rats is generally low in Ly49 receptors, but expresses the rat NKR-P1B PVG receptor (previously termed NKR-P1C). The NKR-P1B 1 NK subset is inhibited by a non-polymorphic target cell ligand, which we have shown here to be a C-type lectin-related molecule (Clr). Clr11 ligates two divergent NKR-P1B alleles as judged by an NFAT-driven reporter assay, and inhibits NK-cell cytotoxicity of NKR-P1B 1 NK cells. Clr11 also interacts with the prototypic NKR-P1A receptor and exerts a stimulatory influence on NK lysis. NKR-P1A and B are encoded by adjacent genes in the proximal part of the NK gene complex and show close sequence homology in their extracellular region. They diverge from another pair, NKR-P1F and -G, which is encoded by a second, distal Nkrp1 gene cluster. NKR-P1F and -G bind an overlapping panel of Clr ligands, but not Clr11. Rat Clr molecules appear to be constitutively expressed by hematopoietic cells; expression in tumor cell lines is more variable. The data show the existence of two phylogenetic groups of NKR-P1 molecules, which demonstrate conservation of ligand-binding properties independent of signaling function.Key words: Cytotoxicity . NK cells . Receptor . Rodent Introduction NK cells express several families of killer cell lectin-like receptors (KLR). These are type II transmembrane proteins encoded by the NK gene complex (NKC), which is located on chromosome 4 in the rat [1,2]. The NKR-P1 molecules (KLRB or CD161) were among the first KLR to be characterized, but their function long remained elusive [3][4][5]. Although the NKR-P1 family has expanded to include both activating and inhibitory members in rodents, it consists of only one member in several other mammalian species, including in human [6]. The nature of their ligands has been controversial [7,8], but it has recently been shown that members of another KLR-related receptor family, the C-type lectin-related (Clr) molecules [9], also termed C-type lectin 2D (CLEC2D), can act as ligands for certain NKR-P1 molecules [10,11]. The Clr gene family also shows considerable expansion in rodents and the Clr genes are interspersed with the Nkrp1 genes in the proximal (centromeric) part of the NKC. A recent analysis concluded that there are 11 Clr/Clec2d genes in the rat BN strain genome, which were numbered consecutively from proximal to distal. One of these (Clr8) is most likely only a gene fragment, which could have been excluded, but we will nevertheless adhere to the Clr numbering suggested by Hao et al. [6].In the mouse, the inhibitory NKR-P1B and -D receptors both bind Clrb (also termed Ocil). Clrb is constitutively expressed by hematopoietic cells and inhibits cytolytic activity of NKR-P1B/ D-expressing NK cells [10,11]. The activating NKR-P1F receptor has been shown to bind another Clr molecule, Clrg, by the use of a reporter assay and soluble recombinant proteins [11] functional consequence of this interaction remains obscure. In human, the NKR-P1A receptor binds a Clr orthologue term...

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Section: Flow Cytometry Mab and Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Two major groups of rat NKR‐P1 receptors can be distinguished based on chromosomal localization, phylogenetic analysis and Clr ligand binding

et al. 2009

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“…It has been assumed that the MoAb 3.2.3 binds the rat equivalent of the human NKR-P1A molecule, but this is still controversial [19,20]. MoAb 3.2.3 strongly reacts with rat NK cells [20,21], while granulocytes [22,23] and a subset of T lymphocytes [24,25] are only weakly 3.2.3-positive. Rat dendritic cells were only recently found to express NKR-P1 [26].…”

Section: Introductionmentioning

confidence: 99%

Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR‐P1 and Reduction of CD43

Scriba

Steiniger

1998

Scand J Immunol

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Scriba A, Grau V, Steiniger B. Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR-P1 and Reduction of CD43. Scand J Immunol 1998;47;332-342 Monocytes and macrophages mediate cytotoxicity after appropriate activation and thus represent effectors secondary to T lymphocytes and natural killer (NK) cells. However, very little is known about the role of activated monocytes in organ allograft rejection. In this study, isogeneic (LEW to LEW) and fully allogeneic (DA to LEW) rat kidneys were grafted to bilaterally nephrectomized recipients. Four days after transplantation a comprehensive sample of leucocytes was recovered by perfusion of the recipients' vasculature with phosphate-buffered saline containing EDTA (PBS/EDTA). Monocytes were enriched by density gradient centrifugation and their physical parameters and immunophenotype were investigated by flow cytometry in comparison with untreated, specified pathogen-free (SPF) LEW rats. Isotransplantation and allotransplantation of kidneys dramatically increased the absolute number of intravascular monocytes in the recipient. Analysis of NKR-P1 (CD161), CD4, CD62L, CD43, CD11a, CD18 and MHC class II expression identified at least two monocyte populations in all experimental groups. In graft recipients it was evident that activated monocytes were able to express and upregulate NKR-P1 and CD8, which have not been detected in these cells to date. If activated monocytes utilize NKR-P1 and CD8, by analogy to NK cells and lymphocytes these cells may be endowed with additional pathways to upregulate cytolytic functions and effect allograft damage. Professor B. Steiniger,

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Natural killer cells and cancer

Brittenden

Heys

Ross

et al. 1996

Cancer

300

160

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NK and LAK cells, through the use of immune biologic modifiers, have been demonstrated to have a therapeutic role in the treatment of human cancers. Further studies are required to determine the optimal dosages and combinations of chemotherapeutic agents, the timing of surgery, and the adjuvant use of immune biologic response modifiers. An increasing awareness and understanding of this field, may allow for the future development of anti-cancer therapies.

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Monoclonal antibody to a triggering structure expressed on rat natural killer cells and adherent lymphokine-activated killer cells.

Cited by 346 publications

References 45 publications

Two major groups of rat NKR‐P1 receptors can be distinguished based on chromosomal localization, phylogenetic analysis and Clr ligand binding

Two major groups of rat NKR‐P1 receptors can be distinguished based on chromosomal localization, phylogenetic analysis and Clr ligand binding

Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR‐P1 and Reduction of CD43

Natural killer cells and cancer

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