guest ::
| Home > Publications database > CD16A Activation of NK Cells Promotes NK Cell Proliferation and Memory-Like Cytotoxicity against Cancer Cells. > print |
| Home > Publications database > CD16A Activation of NK Cells Promotes NK Cell Proliferation and Memory-Like Cytotoxicity against Cancer Cells. > print |
| 001 | 132942 | ||
| 005 | 20240229105040.0 | ||
| 024 | 7 | _ | |a 10.1158/2326-6066.CIR-17-0550 |2 doi |
| 024 | 7 | _ | |a pmid:29514797 |2 pmid |
| 024 | 7 | _ | |a 2326-6066 |2 ISSN |
| 024 | 7 | _ | |a 2326-6074 |2 ISSN |
| 024 | 7 | _ | |a altmetric:34134024 |2 altmetric |
| 037 | _ | _ | |a DKFZ-2018-00581 |
| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Pahl, Jens |0 P:(DE-He78)0f643e43f006f9ce6666909ec4f79a2f |b 0 |e First author |u dkfz |
| 245 | _ | _ | |a CD16A Activation of NK Cells Promotes NK Cell Proliferation and Memory-Like Cytotoxicity against Cancer Cells. |
| 260 | _ | _ | |a Philadelphia, Pa. |c 2018 |b AACR |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1527241143_21565 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a CD16A is a potent cytotoxicity receptor on human natural killer (NK) cells, which can be exploited by therapeutic bispecific antibodies. So far, the effects of CD16A-mediated activation on NK cell effector functions beyond classical antibody-dependent cytotoxicity have remained poorly elucidated. Here, we investigated NK cell responses after exposure to therapeutic antibodies such as the tetravalent bispecific antibody AFM13 (CD30/CD16A), designed for the treatment of Hodgkin lymphoma and other CD30+ lymphomas. Our results reveal that CD16A engagement enhanced subsequent IL2- and IL15-driven NK cell proliferation and expansion. This effect involved the upregulation of CD25 (IL2Rα) and CD132 (γc) on NK cells, resulting in increased sensitivity to low-dose IL2 or to IL15. CD16A engagement initially induced NK cell cytotoxicity. The lower NK cell reactivity observed 1 day after CD16A engagement could be recovered by reculture in IL2 or IL15. After reculture in IL2 or IL15, these CD16A-experienced NK cells exerted more vigorous IFNγ production upon restimulation with tumor cells or cytokines. Importantly, after reculture, CD16A-experienced NK cells also exerted increased cytotoxicity toward different tumor targets, mainly through the activating NK cell receptor NKG2D. Our findings uncover a role for CD16A engagement in priming NK cell responses to restimulation by cytokines and tumor cells, indicative of a memory-like functionality. Our study suggests that combination of AFM13 with IL2 or IL15 may boost NK cell antitumor activity in patients by expanding tumor-reactive NK cells and enhancing NK cell reactivity, even upon repeated tumor encounters. Cancer Immunol Res; 6(5); 517-27. ©2018 AACR. |
| 536 | _ | _ | |a 314 - Tumor immunology (POF3-314) |0 G:(DE-HGF)POF3-314 |c POF3-314 |f POF III |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 700 | 1 | _ | |a Koch, Joachim |b 1 |
| 700 | 1 | _ | |a Götz, Jana |0 P:(DE-He78)63c7f59c86b4d0aea6cb35656305e1a4 |b 2 |u dkfz |
| 700 | 1 | _ | |a Arnold, Annette |0 P:(DE-He78)7c776439971ef21f36ac730cfbff7fff |b 3 |u dkfz |
| 700 | 1 | _ | |a Reusch, Uwe |b 4 |
| 700 | 1 | _ | |a Gantke, Thorsten |b 5 |
| 700 | 1 | _ | |a Rajkovic, Erich |b 6 |
| 700 | 1 | _ | |a Treder, Martin |b 7 |
| 700 | 1 | _ | |a Cerwenka, Adelheid |0 P:(DE-He78)d2b4dd8bdffe4aaa0f5e30e91587766f |b 8 |e Last author |u dkfz |
| 773 | _ | _ | |a 10.1158/2326-6066.CIR-17-0550 |g Vol. 6, no. 5, p. 517 - 527 |0 PERI:(DE-600)2732517-9 |n 5 |p 517 - 527 |t Cancer immunology research |v 6 |y 2018 |x 2326-6074 |
| 909 | C | O | |o oai:inrepo02.dkfz.de:132942 |p VDB |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 0 |6 P:(DE-He78)0f643e43f006f9ce6666909ec4f79a2f |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 2 |6 P:(DE-He78)63c7f59c86b4d0aea6cb35656305e1a4 |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 3 |6 P:(DE-He78)7c776439971ef21f36ac730cfbff7fff |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 8 |6 P:(DE-He78)d2b4dd8bdffe4aaa0f5e30e91587766f |
| 913 | 1 | _ | |a DE-HGF |l Krebsforschung |1 G:(DE-HGF)POF3-310 |0 G:(DE-HGF)POF3-314 |2 G:(DE-HGF)POF3-300 |v Tumor immunology |x 0 |4 G:(DE-HGF)POF |3 G:(DE-HGF)POF3 |b Gesundheit |
| 914 | 1 | _ | |y 2018 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0200 |2 StatID |b SCOPUS |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0300 |2 StatID |b Medline |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0310 |2 StatID |b NCBI Molecular Biology Database |
| 915 | _ | _ | |a JCR |0 StatID:(DE-HGF)0100 |2 StatID |b CANCER IMMUNOL RES : 2015 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0199 |2 StatID |b Thomson Reuters Master Journal List |
| 915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0111 |2 StatID |b Science Citation Index Expanded |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0150 |2 StatID |b Web of Science Core Collection |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1050 |2 StatID |b BIOSIS Previews |
| 915 | _ | _ | |a IF >= 5 |0 StatID:(DE-HGF)9905 |2 StatID |b CANCER IMMUNOL RES : 2015 |
| 920 | 1 | _ | |0 I:(DE-He78)D080-20160331 |k D080 |l Nachwuchsgruppe Angeborene Immunität |x 0 |
| 980 | _ | _ | |a journal |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a I:(DE-He78)D080-20160331 |
| 980 | _ | _ | |a UNRESTRICTED |
| Library | Collection | CLSMajor | CLSMinor | Language | Author |
|---|