InVivoMAb anti-human NKG2D (CD314)

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1D11 BE0351InVivoMAb Antibodies
$150 - $3920 Login for Academic & Non-profit Pricing

About InVivoMAb anti-human NKG2D (CD314)

The 1D11 monoclonal antibody reacts with human NKG2D, a type II transmembrane lectin-like glycoprotein also known as CD314. NKG2D is expressed on NK cells, NKT cells, CD8 T cells, γ/δ T cells, and macrophages. NKG2D has been implicated in anti-tumor surveillance, the immune response against viral infection, and in diabetes progression in NOD mice. Previous studies have shown that 1D11 can block the binding of NKG2D to its ligands or stimulate the function of NKG2D-positive cells.

InVivoMAb anti-human NKG2D (CD314) Specifications

Isotype Mouse IgG1, κ
Immunogen Human NKL cells
Reported Applications
  • in vitro NKG2D blocking
  • Immunoprecipitation
  • Flow cytometry
Formulation
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
Endotoxin
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
Purity
  • >95%
  • Determined by SDS-PAGE
Sterility 0.2 μM filtered
Production Purified from tissue culture supernatant in an animal free facility
Purification Protein G
RRID AB_2894770
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.

Application References

InVivoMAb anti-human NKG2D (CD314)

  • in vitro NKG2D blocking

Pereira, B. I., et al. (2020). “Sestrins induce natural killer function in senescent-like CD8(+) T cells.” Nat Immunol 21(6): 684-694. PubMed

Aging is associated with remodeling of the immune system to enable the maintenance of life-long immunity. In the CD8(+) T cell compartment, aging results in the expansion of highly differentiated cells that exhibit characteristics of cellular senescence. Here we found that CD27(-)CD28(-)CD8(+) T cells lost the signaling activity of the T cell antigen receptor (TCR) and expressed a protein complex containing the agonistic natural killer (NK) receptor NKG2D and the NK adaptor molecule DAP12, which promoted cytotoxicity against cells that expressed NKG2D ligands. Immunoprecipitation and imaging cytometry indicated that the NKG2D-DAP12 complex was associated with sestrin 2. The genetic inhibition of sestrin 2 resulted in decreased expression of NKG2D and DAP12 and restored TCR signaling in senescent-like CD27(-)CD28(-)CD8(+) T cells. Therefore, during aging, sestrins induce the reprogramming of non-proliferative senescent-like CD27(-)CD28(-)CD8(+) T cells to acquire a broad-spectrum, innate-like killing activity.

  • in vitro NKG2D blocking

Parsons, M. S., et al. (2016). “NKG2D Acts as a Co-Receptor for Natural Killer Cell-Mediated Anti-HIV-1 Antibody-Dependent Cellular Cytotoxicity.” AIDS Res Hum Retroviruses 32(10-11): 1089-1096. PubMed

The utility of antibody-dependent cellular cytotoxicity (ADCC) for eliminating HIV-1-infected cells is of much interest for the design of both prophylactic vaccines for HIV-1 prevention and therapeutics to eliminate latently infected cells following reactivation. Significant research has been conducted to understand the antibody specificities involved in anti-HIV-1 ADCC responses. Perhaps equally important as the identity of the antibodies mediating these responses are factors regulating the ability of ADCC effector cells, in particular, natural killer (NK) cells, to respond to antibody-coated target cells. Indeed, a plethora of activating and inhibitory receptors expressed on the surface of NK cells might act in conjunction with CD16 to influence ADCC. As the expression of NKG2D and its ligands has been linked to HIV-1 disease progression, we evaluated if signals through NKG2D were involved in anti-HIV-1 ADCC. Utilizing assays measuring cytolysis, we provide the first data implicating NKG2D in antibody-dependent NK cell responses against a target cell line either pulsed with gp120 or infected with HIV-1. These observations are highly significant for understanding antibody-dependent NK cell responses against HIV-1 and might be useful for optimizing prophylactics and therapeutics aiming to utilize antibodies and optimally functional NK cells to control HIV-1.

  • in vitro NKG2D blocking

Zheng, J., et al. (2015). “The Therapeutic Effect of Pamidronate on Lethal Avian Influenza A H7N9 Virus Infected Humanized Mice.” PLoS One 10(8): e0135999. PubMed

A novel avian influenza virus H7N9 infection occurred among human populations since 2013. Although the lack of sustained human-to-human transmission limited the epidemics caused by H7N9, the late presentation of most patients and the emergence of neuraminidase-resistant strains made the development of novel antiviral strategy against H7N9 in urgent demands. In this study, we evaluated the potential of pamidronate, a pharmacological phosphoantigen that can specifically boost human Vdelta2-T-cell, on treating H7N9 virus-infected humanized mice. Our results showed that intraperitoneal injection of pamidronate could potently decrease the morbidity and mortality of H7N9-infected mice through controlling both viral replication and inflammation in affected lungs. More importantly, pamidronate treatment starting from 3 days after infection could still significantly ameliorate the severity of diseases in infected mice and improve their survival chance, whereas orally oseltamivir treatment starting at the same time showed no therapeutic effects. As for the mechanisms underlying pamidronate-based therapy, our in vitro data demonstrated that its antiviral effects were partly mediated by IFN-gamma secreted from human Vdelta2-T cells. Meanwhile, human Vdelta2-T cells could directly kill virus-infected host cells in a perforin-, granzyme B- and CD137-dependent manner. As pamidronate has been used for osteoporosis treatment for more than 20 years, pamidronate-based therapy represents for a safe and readily available option for clinical trials to treat H7N9 infection.

  • in vitro NKG2D blocking

Groh, V., et al. (2001). “Costimulation of CD8alphabeta T cells by NKG2D via engagement by MIC induced on virus-infected cells.” Nat Immunol 2(3): 255-260. PubMed

NKG2D is an activating receptor that stimulates innate immune responses by natural killer cells upon engagement by MIC ligands, which are induced by cellular stress. Because NKG2D is also present on most CD8alphabeta T cells, it may modulate antigen-specific T cell responses, depending on whether MIC molecules–distant homologs of major histocompatibility complex (MHC) class I with no function in antigen presentation–are induced on the surface of pathogen-infected cells. We found that infection by cytomegalovirus (CMV) resulted in substantial increases in MIC on cultured fibroblast and endothelial cells and was associated with induced MIC expression in interstitial pneumonia. MIC engagement of NKG2D potently augmented T cell antigen receptor (TCR)-dependent cytolytic and cytokine responses by CMV-specific CD28- CD8alphabeta T cells. This function overcame viral interference with MHC class I antigen presentation. Combined triggering of TCR-CD3 complexes and NKG2D induced interleukin 2 production and T cell proliferation. Thus NKG2D functioned as a costimulatory receptor that can substitute for CD28.

  • in vitro NKG2D blocking

  • Immunoprecipitation

  • Flow cytometry

Bauer, S., et al. (1999). “Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA.” Science 285(5428): 727-729. PubMed

Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.