Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors

BCR-ABL1-negative myeloproliferative neoplasms are burdened by a reduced life expectancy mostly due to an increased risk of thrombo-hemorrhagic events, fibrotic progression/leukemic evolution, and infectious complications. In these clonal myeloid malignancies, JAK2V617F is the main driver mutation,...

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Autores principales:	Daniele Cattaneo, Alessandra Iurlo
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	myeloproliferative neoplasms JAK inhibitors ruxolitinib infections immune system Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/f0387f2811bc4960a7bb65e2a6fc62db
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spelling	oai:doaj.org-article:f0387f2811bc4960a7bb65e2a6fc62db2021-11-19T04:38:00ZImmune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors1664-322410.3389/fimmu.2021.750346https://doaj.org/article/f0387f2811bc4960a7bb65e2a6fc62db2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.750346/fullhttps://doaj.org/toc/1664-3224BCR-ABL1-negative myeloproliferative neoplasms are burdened by a reduced life expectancy mostly due to an increased risk of thrombo-hemorrhagic events, fibrotic progression/leukemic evolution, and infectious complications. In these clonal myeloid malignancies, JAK2V617F is the main driver mutation, leading to an aberrant activation of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. Therefore, its inhibition represents an attractive therapeutic strategy for these disorders. Several JAK inhibitors have entered clinical trials, including ruxolitinib, the first JAK1/2 inhibitor to become commercially available for the treatment of myelofibrosis and polycythemia vera. Due to interference with the JAK-STAT pathway, JAK inhibitors affect several components of the innate and adaptive immune systems such as dendritic cells, natural killer cells, T helper cells, and regulatory T cells. Therefore, even though the clinical use of these drugs in MPN patients has led to a dramatic improvement of symptoms control, organ involvement, and quality of life, JAK inhibitors–related loss of function in JAK-STAT signaling pathway can be a cause of different adverse events, including those related to a condition of immune suppression or deficiency. This review article will provide a comprehensive overview of the current knowledge on JAK inhibitors’ effects on immune cells as well as their clinical consequences, particularly with regards to infectious complications.Daniele CattaneoDaniele CattaneoAlessandra IurloFrontiers Media S.A.articlemyeloproliferative neoplasmsJAK inhibitorsruxolitinibinfectionsimmune systemImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	myeloproliferative neoplasms JAK inhibitors ruxolitinib infections immune system Immunologic diseases. Allergy RC581-607
spellingShingle	myeloproliferative neoplasms JAK inhibitors ruxolitinib infections immune system Immunologic diseases. Allergy RC581-607 Daniele Cattaneo Daniele Cattaneo Alessandra Iurlo Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors
description	BCR-ABL1-negative myeloproliferative neoplasms are burdened by a reduced life expectancy mostly due to an increased risk of thrombo-hemorrhagic events, fibrotic progression/leukemic evolution, and infectious complications. In these clonal myeloid malignancies, JAK2V617F is the main driver mutation, leading to an aberrant activation of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. Therefore, its inhibition represents an attractive therapeutic strategy for these disorders. Several JAK inhibitors have entered clinical trials, including ruxolitinib, the first JAK1/2 inhibitor to become commercially available for the treatment of myelofibrosis and polycythemia vera. Due to interference with the JAK-STAT pathway, JAK inhibitors affect several components of the innate and adaptive immune systems such as dendritic cells, natural killer cells, T helper cells, and regulatory T cells. Therefore, even though the clinical use of these drugs in MPN patients has led to a dramatic improvement of symptoms control, organ involvement, and quality of life, JAK inhibitors–related loss of function in JAK-STAT signaling pathway can be a cause of different adverse events, including those related to a condition of immune suppression or deficiency. This review article will provide a comprehensive overview of the current knowledge on JAK inhibitors’ effects on immune cells as well as their clinical consequences, particularly with regards to infectious complications.
format	article
author	Daniele Cattaneo Daniele Cattaneo Alessandra Iurlo
author_facet	Daniele Cattaneo Daniele Cattaneo Alessandra Iurlo
author_sort	Daniele Cattaneo
title	Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors
title_short	Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors
title_full	Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors
title_fullStr	Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors
title_full_unstemmed	Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors
title_sort	immune dysregulation and infectious complications in mpn patients treated with jak inhibitors
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/f0387f2811bc4960a7bb65e2a6fc62db
work_keys_str_mv	AT danielecattaneo immunedysregulationandinfectiouscomplicationsinmpnpatientstreatedwithjakinhibitors AT danielecattaneo immunedysregulationandinfectiouscomplicationsinmpnpatientstreatedwithjakinhibitors AT alessandraiurlo immunedysregulationandinfectiouscomplicationsinmpnpatientstreatedwithjakinhibitors
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Immune Dysregulation and Infectious Complications in MPN Patients Treated With JAK Inhibitors

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