TIM-3 levels correlate with enhanced NK cell cytotoxicity and improved clinical outcome in AML patients

Bibliographic Details
Title: TIM-3 levels correlate with enhanced NK cell cytotoxicity and improved clinical outcome in AML patients
Authors: Jana Rakova, Iva Truxova, Peter Holicek, Cyril Salek, Michal Hensler, Lenka Kasikova, Josef Pasulka, Monika Holubova, Marek Kovar, Daniel Lysak, Justin P. Kline, Zdenek Racil, Lorenzo Galluzzi, Radek Spisek, Jitka Fucikova
Source: OncoImmunology, Vol 10, Iss 1 (2021)
Publisher Information: Taylor & Francis Group, 2021.
Publication Year: 2021
Collection: LCC:Immunologic diseases. Allergy
LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
Subject Terms: co-inhibitory receptor, innate lymphoid cells, lag-3, tigit, vista, Immunologic diseases. Allergy, RC581-607, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
More Details: Accumulating evidence indicates that immune checkpoint inhibitors (ICIs) can restore CD8+ cytotoxic T lymphocyte (CTL) functions in preclinical models of acute myeloid leukemia (AML). However, ICIs targeting programmed cell death 1 (PDCD1, best known as PD-1) and cytotoxic T lymphocyte-associated protein 4 (CTLA4) have limited clinical efficacy in patients with AML. Natural killer (NK) cells are central players in AML-targeting immune responses. However, little is known on the relationship between co-inhibitory receptors expressed by NK cells and the ability of the latter to control AML. Here, we show that hepatitis A virus cellular receptor 2 (HAVCR2, best known as TIM-3) is highly expressed by NK cells from AML patients, correlating with improved functional licensing and superior effector functions. Altogether, our data indicate that NK cell frequency as well as TIM-3 expression levels constitute prognostically relevant biomarkers of active immunity against AML.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2162-402X
2162402X
Relation: https://doaj.org/toc/2162-402X
DOI: 10.1080/2162402X.2021.1889822
Access URL: https://doaj.org/article/7aa2896ab527498bac5610f866169e29
Accession Number: edsdoj.7aa2896ab527498bac5610f866169e29
Database: Directory of Open Access Journals
More Details
ISSN:2162402X
DOI:10.1080/2162402X.2021.1889822
Published in:OncoImmunology
Language:English