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The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox

1
Division of Hematology, Department of Human Pathology in Adulthood and Childhood, University of Messina, 98125 Messina, Italy
2
National Research Council of Italy (CNR)-Institute for Biomedical Research and Innovation (IRIB), 98164 Messina, Italy
3
School and Division of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University Hospital “G. Martino”, Via Consolare Valeria SNC, 98125 Messina, Italy
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2019, 20(20), 5226; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20205226
Received: 16 July 2019 / Revised: 15 October 2019 / Accepted: 16 October 2019 / Published: 22 October 2019
(This article belongs to the Section Molecular Immunology)
Interleukin (IL)-33 is a chromatin-related nuclear interleukin that is a component of IL-1 family. IL-33 production augments the course of inflammation after cell damage or death. It is discharged into the extracellular space. IL-33 is regarded as an “alarmin” able to stimulate several effectors of the immune system, regulating numerous immune responses comprising cancer immune reactions. IL-33 has been demonstrated to influence tumorigenesis. However, as far as this cytokine is concerned, we are faced with what has sometimes been defined as the IL-33 paradox. Several studies have demonstrated a relevant role of IL-33 to numerous malignancies, where it may have pro- and—less frequently—antitumorigenic actions. In the field of hematological malignancies, the role of IL-33 seems even more complex. Although we can affirm the existence of a negative role of IL-33 in Chronic myelogenos leukemia (CML) and in lymphoproliferative diseases and a positive role in pathologies such as Acute myeloid leukemia (AML), the action of IL-33 seems to be multiple and sometimes contradictory within the same pathology. In the future, we will have to learn to govern the negative aspects of activating the IL-33/ST2 axis and exploit the positive ones. View Full-Text
Keywords: alarmin; hematologic malignancies; interleukin 33; immune response; tumorigenesis alarmin; hematologic malignancies; interleukin 33; immune response; tumorigenesis
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MDPI and ACS Style

Allegra, A.; Innao, V.; Tartarisco, G.; Pioggia, G.; Casciaro, M.; Musolino, C.; Gangemi, S. The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox. Int. J. Mol. Sci. 2019, 20, 5226. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20205226

AMA Style

Allegra A, Innao V, Tartarisco G, Pioggia G, Casciaro M, Musolino C, Gangemi S. The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox. International Journal of Molecular Sciences. 2019; 20(20):5226. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20205226

Chicago/Turabian Style

Allegra, Alessandro, Vanessa Innao, Gennaro Tartarisco, Giovanni Pioggia, Marco Casciaro, Caterina Musolino, and Sebastiano Gangemi. 2019. "The ST2/Interleukin-33 Axis in Hematologic Malignancies: The IL-33 Paradox" International Journal of Molecular Sciences 20, no. 20: 5226. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20205226

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