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Titolo:
Elevated circulating levels of soluble interleukin-1 receptor type II during interleukin-2 immunotherapy
Autore:
Vannier, E; Kaser, A; Atkins, MB; Fantuzzi, G; Dinarello, CA; Mier, JW; Tilg, H;
Indirizzi:
NewUSAgland Med Ctr, Dept Med, Div Geog Med & Infect Dis, Boston, MA 02111New England Med Ctr Boston MA USA 02111 ed & Infect Dis, Boston, MA 02111 Tufts Univ, Sch Med, Boston, MA 02111 USA Tufts Univ Boston MA USA 02111Tufts Univ, Sch Med, Boston, MA 02111 USA Univk,nnsbruck Hosp, Dept Med, Div Gastroenterol & Hepatol, A-6020 Innsbruc Univ Innsbruck Hosp Innsbruck Austria A-6020 & Hepatol, A-6020 Innsbruc HarvardOncol, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med,Div HematolHarvard Univ Boston MA USA srael Deaconess Med Ctr, Dept Med,Div Hematol Univ Colorado, Hlth Sci Ctr, Dept Med, Div Infect Dis, Denver, CO 80262 USA Univ Colorado Denver CO USA 80262 d, Div Infect Dis, Denver, CO 80262 USA
Titolo Testata:
EUROPEAN CYTOKINE NETWORK
fascicolo: 1, volume: 10, anno: 1999,
pagine: 37 - 41
SICI:
1148-5493(199903)10:1<37:ECLOSI>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; MESSENGER-RNA EXPRESSION; HIGH-DOSE INTERLEUKIN-2; IL-1 RECEPTOR; ANTIINFLAMMATORY CYTOKINE; VISCERAL ISCHEMIA; DECOY RECEPTOR; FACTOR TNF; INDUCTION; ANTAGONIST;
Keywords:
cancer; IL-2; IL-6; immunotherapy; soluble IL-1 receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Tilg, H Dept Med, Anichstr 35, A-6020 Innsbruck, Austria Dept Med Anichstr35 Innsbruck Austria A-6020 Innsbruck, Austria
Citazione:
E. Vannier et al., "Elevated circulating levels of soluble interleukin-1 receptor type II during interleukin-2 immunotherapy", EUR CYTOKIN, 10(1), 1999, pp. 37-41

Abstract

Interleukin-1 (IL-1) is a critical mediator of inflammation, Two naturallyoccurring IL-1 antagonists have been described, namely the IL-1 receptor antagonist (IL-1Ra) and the IL-1 receptor type II (IL-1RII), IL-1RII does not transmit a signal upon binding of IL-1, but competes with the signaling of IL-1RI. for binding of IL-1, Shedding of IL-1RII yields the soluble IL-1 receptor type II (IL-1sRII) which retains the ability of membrane-bound IL-1RII to bind IL-1 beta avidly,but binds IL-1Ra and IL-1 alpha with low affinity, In contrast, IL-1sRI retains the ability of membrane-bound IL-1RI to bind IL-1Ra and IL-1 alpha with high affinity, but binds IL-1 beta poorly, We have previously shown that immunotherapy with IL-2 or IL-6 in cancer patients is associated with a dramatic increase in IL-1Ra plasma levels. In the present study, plasma levels of soluble IL-1 receptors were monitored in healthy individuals and cancer patients. In healthy controls, the mean IL-1sRII level was 4.76 +/- 0.16 ng/ml, IL-1sRII levels in cancer patients werecomparable to those measured in healthy controls. IL-1sRII levels did not vary during the first 52 hours after initiation of IL-2 therapy, but increased significantly thereafter to reach 9.56 +/- 1.16 ng/ml on day 5, In contrast, IL-6 immunotherapy with a 5-day continuous infusion did not trigger an increase in IL-1sRII levels. IL-1sRI levels did not increase during immunotherapy with IL-2 or IL-6. Our results indicate that IL-1sRII, unlike IL-1Ra, remains a modest, natural, anti-inflammatory mechanism triggered by immunotherapy with IL-2, but not with IL-6.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 22:10:47