Abstract
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.
Highlights
Interleukin (IL)-33 is a component of the IL-1 family, cytokines that maintain a structure of β-trefoil folds containing 12 antiparallel β-strands that are organized in a three-fold symmetric configuration [1]
While these results suggest a possible therapeutic advantage in stopping IL-33/ST2 signaling in Myeloproliferative neoplasms (MPNs), other studies should determine the role of this system for disease progression and drug resistance in MPN subjects
Our study described the existence of an inverse correlation between plasma levels of IL-33 and CD20 expression, and IL-33 seems to be able to modify the expression of CD20
Summary
Interleukin (IL)-33 is a component of the IL-1 family, cytokines that maintain a structure of β-trefoil folds containing 12 antiparallel β-strands that are organized in a three-fold symmetric configuration [1]. It is recognized that this cytokine is a chromatin-related nuclear interleukin, and that connecting to histones is crucial for IL-33 action [3]. Nuclear IL-33 can act as a transcriptional repressor when overexpressed in cells [4]. OMrdoirnegovtoert,hiencfleallmtympaetoanryd pthroetdeiasseeassefr, oamndmdaifsfterceenlltsimanmduonteheerffceecltlssacraencatruasnesdfobrym ftuhlel-dleinffgerthenItLm-3o3leicnutolessh[1o5r,t1e6r].sMtruocretuorveesr,(i1n8f–la2m1 mkDatao)rywphroosteeaascetsiofnroims 3m0a-fsotlcdelmls oarnedpoothteenrtcethllasncatnhe fturalln-lsefnogrmth ffuolrlm-le.nHgtohwILev-3e3r,inthtoe sshhoorrtteerr sftorrumctudroeess(n18o–t2p1akssDian)two hthoesenaucctlieounsiass3i0t-fdooldesmnoortehpaovteentht e nuclear localization signal present in full-length IL-33 [10,17,18,19]. The shorter form does not pass into the nucleus as it does not have the nuclear localization signal present in full-length IL-33 [10,17,18,19]
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