| Literature DB >> 35507686 |
Paul M Maciocia1, Patrycja A Wawrzyniecka1, Nicola C Maciocia1, Amy Burley1, Thaneswari Karpanasamy1, Sam Devereaux1, Malika Hoekx1, David O'Connor1, Theresa Leon1, Tanya Rapoz-D'Silva1, Rachael Pocock1, Sunniyat Rahman1, Giuseppe Gritti2, Diana C Yánez3, Susan Ross3, Tessa Crompton3, Owen Williams3, Lydia Lee1, Martin A Pule1, Marc R Mansour1,3.
Abstract
T cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of immature T lymphocytes, associated with higher rates of induction failure compared with those in B cell acute lymphoblastic leukemia. The potent immunotherapeutic approaches applied in B cell acute lymphoblastic leukemia, which have revolutionized the treatment paradigm, have proven more challenging in T-ALL, largely due to a lack of target antigens expressed on malignant but not healthy T cells. Unlike B cell depletion, T-cell aplasia is highly toxic. Here, we show that the chemokine receptor CCR9 is expressed in >70% of cases of T-ALL, including >85% of relapsed/refractory disease, and only on a small fraction (<5%) of normal T cells. Using cell line models and patient-derived xenografts, we found that chimeric antigen receptor (CAR) T-cells targeting CCR9 are resistant to fratricide and have potent antileukemic activity both in vitro and in vivo, even at low target antigen density. We propose that anti-CCR9 CAR-T cells could be a highly effective treatment strategy for T-ALL, avoiding T cell aplasia and the need for genome engineering that complicate other approaches.Entities:
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Year: 2022 PMID: 35507686 DOI: 10.1182/blood.2021013648
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 25.476