title: Analysis of interleukin (IL)-1beta IL-1 receptor antagonist, soluble IL-1 receptor type II and IL-1 accessory protein in HCV-associated lymphoproliferative disorders.
abstract: Hepatitis C virus (HCV) causes hepatitis, liver cirrhosis and hepatocellular carcinoma, and may also induce type II mixed cryoglobulinemia syndrome (MC), a disease characterized by clonal B-cell lymphoproliferations that can evolve into non-Hodgkin's lymphoma (NHL). Interleukin-1 (IL-1) is a cytokine that plays an important role in initiating the cascade of events of immunoinflammatory responses through costimulation of T lymphocytes, B-cell proliferation, induction of adhesion molecules and stimulation of the production of other inflammatory cytokines. The role of IL-1 in immunoinflammatory responses is highlighted by the presence of endogenous regulators (IL-1 receptor antagonist, soluble receptors type 1 and II, human IL-1 accessory protein) that, when secreted into the blood stream may serve as endogenous regulators of IL-1 action. The aim of this study was to evaluate whether abnormalities in the blood levels of IL-1beta IL-1 receptor antagonist, soluble IL-1 receptor type II and human IL-1 accessory protein in HCV+ patients are associated with development of MC and/or NHL. Relative to healthy controls, we observed: i) an increase in the circulating levels of IL-1beta in HCV+ patients simultaneously affected by NHL; ii) increased levels of IL-1 accessory protein in patients singly infected by HCV; iii) increase of IL-1 receptor antagonist in HCV+ patients and in those affected also by NHL with or without MC; iv) a homogeneous increase of sIL-1R type II in all the subgroup of patients. These data indicate that an attempt to increased circulating levels of IL-1 inhibitors occurs at different extent in the course of HCV infection as well as in its progression to NHL and/or MC.
authors.affiliation: Department of Biomedical Sciences, University of Catania, 95124 Catania, Italy. mlibra@unict.it
authors.forename: Massimo
authors.initials: M
authors.lastname: Libra
authors.forename: Katia
authors.initials: K
authors.lastname: Mangano
authors.forename: Massimiliano
authors.initials: M
authors.lastname: Anzaldi
authors.forename: Cinzia
authors.initials: C
authors.lastname: Quattrocchi
authors.forename: Marco
authors.initials: M
authors.lastname: Donia
authors.forename: Roberto
authors.initials: R
authors.lastname: di Marco
authors.forename: Santo
authors.initials: S
authors.lastname: Signorelli
authors.forename: Guido
authors.initials: G
authors.lastname: Scalia
authors.forename: Anna L
authors.initials: AL
authors.lastname: Zignego
authors.forename: Valli
authors.initials: V
authors.lastname: de Re
authors.forename: Maria C
authors.initials: MC
authors.lastname: Mazzarino
authors.forename: Ferdinando
authors.initials: F
authors.lastname: Nicoletti
mesh_terms: D016022:Case-Control Studies; D003449:Cryoglobulinemia / Q000097:blood* / Q000821:virology; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000821:virology; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000097:blood*; D053577:Interleukin-1 Receptor Accessory Protein; D007963:Leukocytes, Mononuclear / Q000821:virology; D016393:Lymphoma, B-Cell / Q000097:blood* / Q000150:complications / Q000821:virology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D017472:Receptors, Interleukin-1 / Q000097:blood*; D053574:Receptors, Interleukin-1 Type II; D012795:Sialoglycoproteins / Q000097:blood*
chemical_list: C507765:IL1RAP protein, human; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D053577:Interleukin-1 Receptor Accessory Protein; D012367:RNA, Viral; D017472:Receptors, Interleukin-1; D053574:Receptors, Interleukin-1 Type II; D012795:Sialoglycoproteins