IL1R8 Deficiency Drives Autoimmunity-Associated Lymphoma Development.

Details

Serval ID
serval:BIB_2F6A0243D9DA
Type
Article: article from journal or magazin.
Collection
Publications
Title
IL1R8 Deficiency Drives Autoimmunity-Associated Lymphoma Development.
Journal
Cancer immunology research
Author(s)
Massara Matteo
Publication state
Published
Issued date
24/04/2019
Language
english
Abstract
Chronic inflammation, including that driven by autoimmunity, is associated with the 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 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 the aging of IL1R8-deficient lpr mice, observing an increased lymphoid cell expansion that evolved to diffuse large B-cell lymphoma (DLBCL). Molecular and gene-expression analyses showed that the NF-κB pathway was constitutively activated in Il1r8 -/-/lpr B splenocytes. In human DLBCL, IL1R8 had reduced expression compared with normal B cells, and higher IL1R8 expression was associated with a better outcome. Thus, IL1R8 silencing is associated with increased lymphoproliferation and transformation in the pathogenesis of B-cell lymphomas associated with autoimmunity.
Pubmed
Create date
16/01/2020 14:02
Last modification date
02/11/2022 6:41
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