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Article: Ex vivo activation of CD56+ immune cells that eradicate neuroblastoma

TitleEx vivo activation of CD56<sup>+</sup> immune cells that eradicate neuroblastoma
Authors
Issue Date2013
Citation
Cancer Research, 2013, v. 73, n. 8, p. 2608-2618 How to Cite?
AbstractDespite the use of intensive contemporary multimodal therapy, the overall survival of patients with high-risk neuroblastoma is still less than 50%. Therefore, immunotherapy without cross-resistance and overlapping toxicity has been proposed. In this study, we report the development of a novel strategy to specifically activate and expand human CD56+ (NCAM1) natural killer (NK) immune cells from normal donors and patients with neuroblastoma. Enriched CD56+ cells from peripheral blood were mixed with CD56+ fraction at 1:1 ratio and cultured in the presence of OKT3, interleukin (IL)-2, and -15 for five days and then without OKT3 for 16 more days. The final products contained more than 90% CD56+ cells and could kill neuroblastoma cells effectively that were originally highly resistant to nonprocessed NK cells. Mechanistically, cytolysis of neuroblastoma was mediated through natural cytotoxicity receptor (NCR), DNAX accessory molecule-1 (DNAM-1; CD226), perforin, and granzyme B. Successful clinical scale-up in a good manufacturing practices (GMP)-compliant bioreactor yielded effector cells that in a neuroblastoma xenograft model slowed tumor growth and extended survival without GVHD. Investigation of CD56+ cells from patients with neuroblastoma revealed a similar postactivation phenotype and lytic activity. Our findings establish a novel and clinically expedient strategy to generate allogeneic or autologous CD56+ cells that are highly cytotoxic against neuroblastoma with minimal risk of GVHD. © 2013 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/294464
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRujkijyanont, Piya-
dc.contributor.authorChan, Wing Keung-
dc.contributor.authorEldridge, Paul W.-
dc.contributor.authorLockey, Timothy-
dc.contributor.authorHolladay, Martha-
dc.contributor.authorRooney, Barbara-
dc.contributor.authorDavidoff, Andrew M.-
dc.contributor.authorLeung, Wing-
dc.contributor.authorVong, Queenie-
dc.date.accessioned2020-12-03T08:22:48Z-
dc.date.available2020-12-03T08:22:48Z-
dc.date.issued2013-
dc.identifier.citationCancer Research, 2013, v. 73, n. 8, p. 2608-2618-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/294464-
dc.description.abstractDespite the use of intensive contemporary multimodal therapy, the overall survival of patients with high-risk neuroblastoma is still less than 50%. Therefore, immunotherapy without cross-resistance and overlapping toxicity has been proposed. In this study, we report the development of a novel strategy to specifically activate and expand human CD56+ (NCAM1) natural killer (NK) immune cells from normal donors and patients with neuroblastoma. Enriched CD56+ cells from peripheral blood were mixed with CD56+ fraction at 1:1 ratio and cultured in the presence of OKT3, interleukin (IL)-2, and -15 for five days and then without OKT3 for 16 more days. The final products contained more than 90% CD56+ cells and could kill neuroblastoma cells effectively that were originally highly resistant to nonprocessed NK cells. Mechanistically, cytolysis of neuroblastoma was mediated through natural cytotoxicity receptor (NCR), DNAX accessory molecule-1 (DNAM-1; CD226), perforin, and granzyme B. Successful clinical scale-up in a good manufacturing practices (GMP)-compliant bioreactor yielded effector cells that in a neuroblastoma xenograft model slowed tumor growth and extended survival without GVHD. Investigation of CD56+ cells from patients with neuroblastoma revealed a similar postactivation phenotype and lytic activity. Our findings establish a novel and clinically expedient strategy to generate allogeneic or autologous CD56+ cells that are highly cytotoxic against neuroblastoma with minimal risk of GVHD. © 2013 American Association for Cancer Research.-
dc.languageeng-
dc.relation.ispartofCancer Research-
dc.titleEx vivo activation of CD56<sup>+</sup> immune cells that eradicate neuroblastoma-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-12-3322-
dc.identifier.pmid23440424-
dc.identifier.scopuseid_2-s2.0-84876916221-
dc.identifier.volume73-
dc.identifier.issue8-
dc.identifier.spage2608-
dc.identifier.epage2618-
dc.identifier.eissn1538-7445-
dc.identifier.isiWOS:000317595800023-
dc.identifier.issnl0008-5472-

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