IRIS Institutional Research Information System - AIR Archivio Istituzionale della Ricerca

IRIS è il sistema di gestione integrata dei dati della ricerca (persone, progetti, pubblicazioni, attività) adottato dall'Università degli Studi di Milano.

AIR nasce in UNIMI nel 2006 con lo scopo di raccogliere, documentare e conservare le informazioni sulla produzione scientifica dell'Università degli Studi di Milano e costituisce di fatto l'Anagrafe della ricerca dell'Ateneo.

Chronic inflammation, including that driven by autoimmunity, is associated with development of B-cell lymphomas. IL1R8 is a regulatory receptor belonging to the IL1R family, which negatively regulates NF-κB activation following stimulation of IL1R or Toll-like receptor (TLR) family members. IL1R8-deficiency is associated with the development of severe autoimmune lupus-like disease in lpr mice. We herein investigated whether concomitant exacerbated inflammation and autoimmunity caused by the deficiency of IL1R8 could recapitulate autoimmunity-associated lymphomagenesis. We thus monitored B-cell lymphoma development during aging of IL1R8-deficient lpr mice, observing increased lymphoid cell expansion that evolved to diffuse large B-cell lymphoma (DLBCL). Molecular and gene expression analysis showed that the NF-κB pathway was constitutively activated in Il1r8-/-/lpr B splenocytes. In human DLBCL, IL1R8 had reduced expression compared to normal B cells, and higher IL1R8 expression was associated with better outcome. Thus, IL1R8 silencing is associated with increased lymphoproliferation and transformation in the pathogenesis of B-cell lymphomas associated with autoimmunity.

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