{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,2]],"date-time":"2026-08-02T15:13:09Z","timestamp":1785683589847,"version":"3.56.0"},"reference-count":48,"publisher":"American Society of Hematology","issue":"13","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,9,29]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Adult T-cell leukemia (ATL) is a lymphoid neoplasm caused by human T-cell leukemia virus type 1 (HTLV-1), which encodes the transcriptional activator Tax, which participates in the immortalization of infected T cells. ATL is classified into 4 subtypes: smoldering, chronic, acute, and lymphoma. We determined whether natural killer receptors (NKRs) were expressed in ATL. NKR expression (KIR2DL1\/2DS1, KIR2DL2\/2DL3\/2DS2, KIR3DL2, NKG2A, NKG2C, and NKp46) was assessed in a discovery cohort of 21 ATL, and KIR3DL2 was then assessed in 71 patients with ATL. KIR3DL2 was the only NKR among those studied frequently expressed by acute-type vs lymphoma- and chronic\/smoldering-type ATL (36 of 40, 4 of 16, and 1 of 15, respectively; P = .001), although acute- and lymphoma-type ATL had similar mutation profiles by targeted exome sequencing. The correlation of KIR3DL2 expression with promoter demethylation was determined by microarray-based DNA methylation profiling. To explore the role of HTLV-1, KIR3DL2 and TAX messenger RNA (mRNA) expression levels were assessed by PrimeFlow RNA in primary ATL and in CD4+ T cells infected with HTLV-1 in\u00a0vitro. TAX mRNA and KIR3DL2 protein expressions were correlated on ATL cells. HTLV-1 infection triggered KIR3DL2 by CD4+ cells but Tax alone did not induce KIR3DL2 expression. Ex vivo, autologous, antibody-dependent cell cytotoxicity using lacutamab, a first-in-class anti-KIR3DL2 humanized antibody, selectively killed KIR3DL2+ primary ATL cells ex vivo. To conclude, KIR3DL2 expression is associated with acute-type ATL. Transcription of KIR3DL2 may be triggered by HTLV-1 infection and correlates with hypomethylation of the promoter. The benefit of targeting KIR3DL2 with lacutamab is being further explored in a randomized phase 2 study in peripheral T-cell lymphoma, including ATL (registered on https:\/\/clinicaltrials.gov as #NCT04984837).<\/jats:p>","DOI":"10.1182\/blood.2022016765","type":"journal-article","created":{"date-parts":[[2022,6,10]],"date-time":"2022-06-10T18:52:37Z","timestamp":1654887157000},"page":"1522-1532","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":9,"title":["KIR3DL2 contributes to the typing of acute adult T-cell leukemia and is a potential therapeutic target"],"prefix":"10.1182","volume":"140","author":[{"given":"Morgane","family":"Cheminant","sequence":"first","affiliation":[{"name":"1Clinical Hematology, Necker-Enfants Malades University Hospital, Assistance Publique-H\u00f4pitaux de Paris (AP-HP), Paris, France;"},{"name":"2Laboratory of Hematological Disorders, Institut Imagine, Universit\u00e9 de Paris Cit\u00e9, INSERM 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