Immunomodulatory effect of ibrutinib: Reducing the barrier against fungal infections.
Adenine
/ adverse effects
Agammaglobulinaemia Tyrosine Kinase
/ antagonists & inhibitors
Humans
Invasive Fungal Infections
/ chemically induced
Leukemia, Lymphocytic, Chronic, B-Cell
Neoplasm Proteins
/ antagonists & inhibitors
Piperidines
/ adverse effects
Protein Kinase Inhibitors
/ adverse effects
BTK
Fungal infection
Ibrutinib
Immunomodulation
Journal
Blood reviews
ISSN: 1532-1681
Titre abrégé: Blood Rev
Pays: England
ID NLM: 8708558
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
04
01
2019
revised:
29
05
2019
accepted:
24
10
2019
pubmed:
9
11
2019
medline:
22
1
2021
entrez:
9
11
2019
Statut:
ppublish
Résumé
The Bruton tyrosine kinase (BTK) inhibitor ibrutinib is increasingly used in the treatment of chronic lymphocytic leukemia (CLL). Moreover, very promising results have been reported in other B-cell malignancies, including primary central nervous system lymphoma (PCNSL). Although well-tolerated in the majority of patients, ibrutinib demonstrates in some cases troublesome toxicities, including invasive fungal infections (IFIs). In the present review, we summarize clinical manifestations of IFIs in patients treated with ibrutinib, generally characterized by an early onset, mild clinical manifestations, asymptomatic/low symptomatic pulmonary localization and high incidence of central nervous system (CNS) involvement. IFI risk appears particularly increased in patients receiving ibrutinib associated with other immune modulator agents, especially with steroids or immune-chemotherapy. Moreover, the immunomodulatory effect of ibrutinib is described, pointing the attention on the involvement of specific molecules targeted by ibrutinib in innate and adaptive response to fungal infection. Overall, the findings indicate the ibrutinib may rapidly impair innate immune cell functions, while concomitantly restoring an effective protective potential of adaptive immune compartment. A correct awareness, especially when other predisposing factors are present, is warranted about the potential risk of IFIs in ibrutinib-treated patients.
Identifiants
pubmed: 31699465
pii: S0268-960X(19)30149-3
doi: 10.1016/j.blre.2019.100635
pii:
doi:
Substances chimiques
Neoplasm Proteins
0
Piperidines
0
Protein Kinase Inhibitors
0
ibrutinib
1X70OSD4VX
Agammaglobulinaemia Tyrosine Kinase
EC 2.7.10.2
BTK protein, human
EC 2.7.10.2
Adenine
JAC85A2161
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
100635Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest R.Mar. received research funding from Janssen and Gilead Sci and honoraria from Gilead Sci., Janssen, Abbvie, Roche and Shire. M.L received honoraria from Gilead Sci., MSD, Pfizer, Novartis, Abbvie, Sanofi, Daiichi Sankyo, Jazz Pharmaceuticals. R.Maf. has received speaker fee from Abbvie. L.A. has received travel grant from Abbvie and BMS. Other Authors have nothing to declare.