Dataset related to article "IL1R8 Deficiency Drives Autoimmunity-Associated Lymphoma Development."
| Main Authors: | Riva F, Ponzoni M, Supino D, Bertilaccio MTS, Polentarutti N, Massara M, Pasqualini F, Carriero R, Innocenzi A, Anselmo A, Veliz-Rodriguez T, Simonetti G, Anders HJ, Caligaris-Cappio F, Mantovani A, Muzio M, Garlanda C |
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| Format: | info dataset eJournal |
| Terbitan: |
, 2020
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| Online Access: |
https://zenodo.org/record/3708985 |
Daftar Isi:
- 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.