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Checkpoint inhibition in the treatment of multiple myeloma : A way to boost innate-like T cell anti-tumor function? / Venken, Koen; Favreau, Mérédis; Gaublomme, Djoere; Menu, Eline; Vanderkerken, Karin; Elewaut, Dirk.

In: Molecular Immunology, Vol. 101, 09.2018, p. 521-526.

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@article{0f43a9c776a446c8b557c0716f4d2f2f,
title = "Checkpoint inhibition in the treatment of multiple myeloma: A way to boost innate-like T cell anti-tumor function?",
abstract = "Multiple myeloma (MM) is a progressive monoclonal B cell malignancy, for which survival and progression largely relies on the crosstalk of tumor cells with the bone marrow (BM) microenvironment, inducing immune escape, angiogenesis, bone destruction and drug resistance. Despite great therapeutic advances, most of the MM patients still relapse and remain incurable. Over the past years, immunotherapy has emerged as a new field in cancer therapy. Here, the immune cells of the patients themselves are activated to target the tumor cells. In MM, several effector cells of the immune system are present in the BM microenvironment; unfortunately, they are mostly all functionally impaired. In this review, we focus on the role of innate-like T cells in MM, particularly CD1d- and MR1- restricted T cells such as respectively invariant natural killer T (iNKT) cells and mucosal associated invariant T (MAIT) cells. These cells have the capacity upon activation to rapidly release copious amounts of cytokines affecting a wide range of innate and adaptive immune responses, and could therefore play a key protective role in anti-tumor immunity. We describe recent observations with regard to functional exhaustion of iNKT and MAIT cells in MM pathology and discuss the potential application of checkpoint inhibition as an attractive target for prolonged activation of these immunomodulatory T cells in the treatment of MM.",
keywords = "Checkpoint inhibition, iNKT cells, MAIT cells, Multiple myeloma, Animals, T-Lymphocytes/immunology, Receptors, Leptin/metabolism, Humans, Immunotherapy, Multiple Myeloma/immunology, Immunity, Innate, Natural Killer T-Cells/metabolism",
author = "Koen Venken and M{\'e}r{\'e}dis Favreau and Djoere Gaublomme and Eline Menu and Karin Vanderkerken and Dirk Elewaut",
note = "Copyright {\circledC} 2018 Elsevier Ltd. All rights reserved.",
year = "2018",
month = "9",
doi = "10.1016/j.molimm.2018.08.019",
language = "English",
volume = "101",
pages = "521--526",
journal = "Molecular Immunology",
issn = "0161-5890",
publisher = "Elsevier Limited",

}

RIS

TY - JOUR

T1 - Checkpoint inhibition in the treatment of multiple myeloma

T2 - A way to boost innate-like T cell anti-tumor function?

AU - Venken, Koen

AU - Favreau, Mérédis

AU - Gaublomme, Djoere

AU - Menu, Eline

AU - Vanderkerken, Karin

AU - Elewaut, Dirk

N1 - Copyright © 2018 Elsevier Ltd. All rights reserved.

PY - 2018/9

Y1 - 2018/9

N2 - Multiple myeloma (MM) is a progressive monoclonal B cell malignancy, for which survival and progression largely relies on the crosstalk of tumor cells with the bone marrow (BM) microenvironment, inducing immune escape, angiogenesis, bone destruction and drug resistance. Despite great therapeutic advances, most of the MM patients still relapse and remain incurable. Over the past years, immunotherapy has emerged as a new field in cancer therapy. Here, the immune cells of the patients themselves are activated to target the tumor cells. In MM, several effector cells of the immune system are present in the BM microenvironment; unfortunately, they are mostly all functionally impaired. In this review, we focus on the role of innate-like T cells in MM, particularly CD1d- and MR1- restricted T cells such as respectively invariant natural killer T (iNKT) cells and mucosal associated invariant T (MAIT) cells. These cells have the capacity upon activation to rapidly release copious amounts of cytokines affecting a wide range of innate and adaptive immune responses, and could therefore play a key protective role in anti-tumor immunity. We describe recent observations with regard to functional exhaustion of iNKT and MAIT cells in MM pathology and discuss the potential application of checkpoint inhibition as an attractive target for prolonged activation of these immunomodulatory T cells in the treatment of MM.

AB - Multiple myeloma (MM) is a progressive monoclonal B cell malignancy, for which survival and progression largely relies on the crosstalk of tumor cells with the bone marrow (BM) microenvironment, inducing immune escape, angiogenesis, bone destruction and drug resistance. Despite great therapeutic advances, most of the MM patients still relapse and remain incurable. Over the past years, immunotherapy has emerged as a new field in cancer therapy. Here, the immune cells of the patients themselves are activated to target the tumor cells. In MM, several effector cells of the immune system are present in the BM microenvironment; unfortunately, they are mostly all functionally impaired. In this review, we focus on the role of innate-like T cells in MM, particularly CD1d- and MR1- restricted T cells such as respectively invariant natural killer T (iNKT) cells and mucosal associated invariant T (MAIT) cells. These cells have the capacity upon activation to rapidly release copious amounts of cytokines affecting a wide range of innate and adaptive immune responses, and could therefore play a key protective role in anti-tumor immunity. We describe recent observations with regard to functional exhaustion of iNKT and MAIT cells in MM pathology and discuss the potential application of checkpoint inhibition as an attractive target for prolonged activation of these immunomodulatory T cells in the treatment of MM.

KW - Checkpoint inhibition

KW - iNKT cells

KW - MAIT cells

KW - Multiple myeloma

KW - Animals

KW - T-Lymphocytes/immunology

KW - Receptors, Leptin/metabolism

KW - Humans

KW - Immunotherapy

KW - Multiple Myeloma/immunology

KW - Immunity, Innate

KW - Natural Killer T-Cells/metabolism

UR - http://www.scopus.com/inward/record.url?scp=85052209009&partnerID=8YFLogxK

U2 - 10.1016/j.molimm.2018.08.019

DO - 10.1016/j.molimm.2018.08.019

M3 - Article

C2 - 30153633

VL - 101

SP - 521

EP - 526

JO - Molecular Immunology

JF - Molecular Immunology

SN - 0161-5890

ER -

ID: 39412548