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IL1R8 Deficiency Drives Autoimmunity-Associated Lymphoma Development.
Federica Riva1,2, Maurilio Ponzoni3, Domenico Supino2
1Department of Veterinary Medicine, University of Milan, Milan, Italy.
Cancer Immunology Research
|April 26, 2019
Summary
Interleukin-1 receptor 8 (IL1R8) deficiency exacerbates autoimmune disease and promotes B-cell lymphoma development. Reduced IL1R8 expression in human diffuse large B-cell lymphoma (DLBCL) correlates with poorer outcomes, suggesting IL1R8
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Chronic inflammation and autoimmunity are linked to B-cell lymphoma development.
- Interleukin-1 receptor 8 (IL1R8) negatively regulates NF-κB signaling.
- IL1R8 deficiency causes severe autoimmune lupus-like disease in mice.
Purpose of the Study:
- To investigate if IL1R8 deficiency-driven inflammation and autoimmunity can cause lymphomagenesis.
- To explore the role of IL1R8 in autoimmunity-associated B-cell lymphomas.
Main Methods:
- Monitoring B-cell lymphoma development in aging IL1R8-deficient lpr mice.
- Conducting molecular and gene-expression analyses on splenocytes.
- Analyzing IL1R8 expression in human diffuse large B-cell lymphoma (DLBCL) samples.
Main Results:
- IL1R8-deficient lpr mice developed diffuse large B-cell lymphoma (DLBCL).
- Constitutive NF-κB pathway activation was observed in Il1r8-/-/lpr B splenocytes.
- Human DLBCL showed reduced IL1R8 expression, with higher levels correlating to better outcomes.
Conclusions:
- IL1R8 deficiency promotes lymphoproliferation and lymphoma development in the context of autoimmunity.
- IL1R8 acts as a tumor suppressor in autoimmunity-associated B-cell lymphomas.
- IL1R8 silencing is implicated in the pathogenesis of B-cell lymphomas.
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