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000282728 037__ $$aDKFZ-2023-01854
000282728 041__ $$aEnglish
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000282728 1001_ $$0P:(DE-He78)115d8608c9bd87a110fc1d05f12d8148$$aKaidun, Polina$$b0$$udkfz
000282728 245__ $$aTargeting NKG2DL with Bispecific NKG2D-CD16 and NKG2D-CD3 Fusion Proteins on Triple-Negative Breast Cancer.
000282728 260__ $$aBasel$$bMolecular Diversity Preservation International$$c2023
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000282728 520__ $$aTriple-negative breast cancer (TNBC) is a particularly aggressive subtype of breast cancer with a poor response rate to conventional systemic treatment and high relapse rates. Members of the natural killer group 2D ligand (NKG2DL) family are expressed on cancer cells but are typically absent from healthy tissues; thus, they are promising tumor antigens for novel immunotherapeutic approaches. We developed bispecific fusion proteins (BFPs) consisting of the NKG2D receptor domain targeting multiple NKG2DLs, fused to either anti-CD3 (NKG2D-CD3) or anti-CD16 (NKG2D-CD16) Fab fragments. First, we characterized the expression of the NKG2DLs (MICA, MICB, ULBP1-4) on TNBC cell lines and observed the highest surface expression for MICA and ULBP2. Targeting TNBC cells with NKG2D-CD3/CD16 efficiently activated both NK and T cells, leading to their degranulation and cytokine release and lysis of TNBC cells. Furthermore, PBMCs from TNBC patients currently undergoing chemotherapy showed significantly higher NK and T cell activation and tumor cell lysis when stimulated with NKG2D-CD3/CD16. In conclusions, BFPs activate and direct the NK and T cells of healthy and TNBC patients against TNBC cells, leading to efficient eradication of tumor cells. Therefore, NKG2D-based NK and T cell engagers could be a valuable addition to the treatment options for TNBC patients.
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000282728 650_7 $$2Other$$aNK cell
000282728 650_7 $$2Other$$aNKG2D
000282728 650_7 $$2Other$$aT cell
000282728 650_7 $$2Other$$aTNBC
000282728 650_7 $$2Other$$abispecific
000282728 650_7 $$2Other$$abreast cancer
000282728 650_7 $$2Other$$afusion protein
000282728 650_7 $$2Other$$aimmunotherapy
000282728 650_7 $$2NLM Chemicals$$aNK Cell Lectin-Like Receptor Subfamily K
000282728 650_7 $$2NLM Chemicals$$aLigands
000282728 650_2 $$2MeSH$$aHumans
000282728 650_2 $$2MeSH$$aTriple Negative Breast Neoplasms: drug therapy
000282728 650_2 $$2MeSH$$aTriple Negative Breast Neoplasms: genetics
000282728 650_2 $$2MeSH$$aNK Cell Lectin-Like Receptor Subfamily K: genetics
000282728 650_2 $$2MeSH$$aLigands
000282728 650_2 $$2MeSH$$aAdministration, Cutaneous
000282728 650_2 $$2MeSH$$aAggression
000282728 7001_ $$0P:(DE-He78)21a98c2d59f71b49ab88e8dbb925e84f$$aHolzmayer, Samuel$$b1$$udkfz
000282728 7001_ $$0P:(DE-HGF)0$$aGreiner, Sarah M$$b2
000282728 7001_ $$0P:(DE-HGF)0$$aSeller, Anna$$b3
000282728 7001_ $$00000-0001-6688-7351$$aTegeler, Christian M$$b4
000282728 7001_ $$0P:(DE-He78)a2cea18c82441ff1f96b2152b3de09d9$$aHagelstein, Ilona$$b5
000282728 7001_ $$0P:(DE-HGF)0$$aMauermann, Jonas$$b6
000282728 7001_ $$00000-0002-8063-2053$$aEngler, Tobias$$b7
000282728 7001_ $$aKoch, André$$b8
000282728 7001_ $$00000-0003-1227-1118$$aHartkopf, Andreas D$$b9
000282728 7001_ $$0P:(DE-He78)15af5d9d6d8f165d5ff4dd165ffecb22$$aSalih, Helmut$$b10$$udkfz
000282728 7001_ $$0P:(DE-He78)a0dc738d8503fa7bfba31420283a45eb$$aMärklin, Melanie$$b11$$udkfz
000282728 773__ $$0PERI:(DE-600)2019364-6$$a10.3390/ijms241713156$$gVol. 24, no. 17, p. 13156 -$$n17$$p13156$$tInternational journal of molecular sciences$$v24$$x1422-0067$$y2023
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