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ADAM10 OR ADAM17 and NK cell

Dang-Huan Pham, Ju-Sun Kim, Sang-Ki Kim, Dong-Jun Shin, Nguyen-Thanh-Tung Uong, Hoon Hyun, Mee Sun Yoon, Sin Jae Kang, Young Jae Ryu, Jin Seong Cho, Jung Han Yoon, Ji Shin Lee, Duck Cho, Soo-Hyeon Lee, Min Ho Park
BACKGROUND/AIM: The inhibition of a disintegrin and metalloproteinase (ADAM) has the potential to become a novel approach for natural killer (NK) cell-based cancer immunotherapy. Thus, the aim of this study was to investigate the influence of ADAM10 and ADAM17 inhibitors on expanded NK cell to enhance antibody-dependent cellular cytotoxicity (ADCC) in breast cancer cell lines. MATERIALS AND METHODS: NK cells were expanded in medium supplemented with an ADAM10 or ADAM17 inhibitor to prevent the shedding of soluble CD16/FcγRIII...
October 2017: Anticancer Research
Kensaku Okada, Hiroki Chikumi, Miyako Takata, Kosuke Yamaguchi, Haruhiko Makino, Tsuyoshi Kitaura, Masaki Nakamoto, Akira Yamasaki, Tadashi Igishi, Naoto Burioka, Eiji Shimizu
BACKGROUND: Clarithromycin is a macrolide antibiotic that possesses anti-inflammatory and immunomodulatory properties. Although recent data suggests that macrolide antibiotics enhance Pseudomonas aeruginosa clearance from the lung, involving natural killer (NK) T cells in this process by activating the NKG2D-NKG2D ligand system, the precise underlying mechanism is still unclear. In this study, we examined the effect of clarithromycin on a potent NKG2D ligand, UL16-binding protein 2 (ULBP2), in the lung and its shedding mechanism...
March 2015: Yonago Acta Medica
Laurie Lajoie, Nicolas Congy-Jolivet, Armelle Bolzec, Valérie Gouilleux-Gruart, Elodie Sicard, Hsueh Cheng Sung, Frank Peiretti, Thierry Moreau, Henri Vié, Béatrice Clémenceau, Gilles Thibault
FcγRIIIA/CD16A, the low-affinity receptor for the IgG Fc portion expressed on human CD56(dim) NK cells and involved in Ab-dependent cell cytotoxicity, is shed upon NK cell activation. We found that recombinant a disintegrin and metalloprotease (ADAM) 17 cleaved the ectodomain of FcγRIIIA/CD16A and a peptide for which the sequence encompasses aa 191-201 of the FcγRIIIA/CD16A stalk region but not ADAM10. MALDI-TOF analysis revealed that the peptide was cleaved between Ala(195) and Val(196) (i.e., 1 aa upstream of the expected position)...
January 15, 2014: Journal of Immunology: Official Journal of the American Association of Immunologists
Fabian Wolpert, Isabel Tritschler, Alexander Steinle, Michael Weller, Günter Eisele
BACKGROUND: There are emerging reports that the family of a disintegrin and metalloproteinases (ADAM) are involved in the maintenance of the malignant phenotype of glioblastomas. Notably, ADAM proteases 10 and 17 might impair the immune recognition of glioma cells via the activating immunoreceptor NKG2D by cleavage of its ligands from the cell surface. Glioblastoma-initiating cells (GIC) with stem cell properties have been identified as an attractive target for immunotherapy. However, GIC immunogenicity seems to be low...
March 2014: Neuro-oncology
Guranda Chitadze, Marcus Lettau, Jaydeep Bhat, Daniela Wesch, Alexander Steinle, Daniel Fürst, Joannis Mytilineos, Holger Kalthoff, Ottmar Janssen, Hans-Heinrich Oberg, Dieter Kabelitz
The interaction of the MHC class I-related chain molecules A and B (MICA and MICB) with the corresponding natural killer group 2, member D (NKG2D) receptor triggers cytotoxic effector activity of natural killer cells and certain T-cell subsets and provides a costimulatory signal for cytokine production. Thus, the presence of MICA/B on transformed cells contributes to tumor immunosurveillance. Consequently, the proteolytic cleavage of MICA/B is regarded as an important immune escape mechanism of various cancer cells...
October 1, 2013: International Journal of Cancer. Journal International du Cancer
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