期刊
BLOOD
卷 129, 期 5, 页码 582-586出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2016-07-731091
关键词
-
类别
资金
- Ministero della Salute [GR-2010-2313609, RF-2009-1548666]
- Associazione Italiana per la Ricerca sul Cancro (AIRC), Milan, Italy [IG 14797-2013]
- AIRC [MCO1007]
- Associazione Italiana Lotta alle Leucemie
- Linfoma e Mieloma-Sezione 'Luciano Pavarotti'-Modena-ONLUS
- Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Policlinico SanMatteo [08069113, 08045801/10, 08045801/1]
Although the emergence of bone marrow (BM)-resident p(190) BCR-ABL-specific T lymphocytes has been correlated with hematologic and cytogenetic remissions in patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) undergoing maintenance tyrosine-kinase inhibitor treatment, little is known about the possibility of culturing these cells ex vivo and using them in T-cell therapy strategies. Weinvestigated the feasibility of expanding/priming p(190) BCR-ABL-specificT cells in vitro by stimulation with dendritic cells pulsed with p(190) BCR-ABL peptides derived from the BCR-ABLjunctional regionandalternative splicing, and of adoptively administering them to patients with relapsed disease. We report on the feasibility of producing clinical-grade BCR-ABL-specific cytotoxic T lymphocytes (CTLs), endowed with antileukemia activity, from Ph+ ALL patients and healthy donors. We treated 3 patients with Ph+ ALL with autologous or allogeneic p(190) BCR-ABL-specific CTLs. No postinfusion toxicity was observed, except for a grade II skin graft-versus-host disease in the patient treated for hematologic relapse. All patients achieved a molecular or hematologic complete remission (CR) after T-cell therapy, upon emergence of p(190) BCR-ABL-specific T cells in the BM. Our results show that p(190) BCR-ABL-specific CTLs are capable of controlling treatment-refractory Ph+ ALL in vivo, and support the development of adoptive immunotherapeutic approaches with BCR-ABL CTLs in Ph+ ALL.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据