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Interferon Lambda Regulates Cellular and Humoral Immunity in Pristane-Induced Lupus
Tom Aschman1,2,3, Sandra Schaffer1, Stylianos Iason Biniaris Georgallis1,3,4
1Department of Rheumatology and Clinical Immunology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg im Breisgau, Germany.
International Journal of Molecular Sciences
|November 13, 2021
Summary
Type III interferons accelerate autoimmune disease development in lupus models. Blocking type III interferon signaling improves survival and reduces inflammation in mice with systemic lupus erythematosus (SLE).
Area of Science:
- Immunology
- Autoimmunity
- Molecular Biology
Background:
- Type I interferons are crucial in systemic lupus erythematosus (SLE).
- Type III interferons (IFN-λ), though less studied in lupus, show potential in regulating immune responses and are elevated in autoimmune diseases.
- Their specific role in lupus pathogenesis remains unclear.
Purpose of the Study:
- To investigate the role of type III interferons in the pristane-induced lupus model.
- To determine the impact of defective type III interferon receptor signaling on disease development and immune cell infiltration.
Main Methods:
- Utilized the pristane-induced lupus mouse model.
- Compared disease progression in wild-type mice versus mice lacking the type III interferon receptor (Ifnlr1-/-).
- Assessed survival rates, autoantibody titers, lipogranuloma formation, and immune cell populations in kidneys and circulation.
Main Results:
- Mice lacking the type III interferon receptor (Ifnlr1-/-) exhibited increased survival, reduced lipogranuloma formation, and lower anti-dsDNA autoantibody titers.
- These mice also showed decreased inflammatory mononuclear phagocytes and cNK cells in the kidneys.
- Systemic analysis revealed reduced circulating B cells and monocytes in Ifnlr1-/- mice.
Conclusions:
- Type III interferons play a significant role in the pathogenesis of pristane-induced murine autoimmunity.
- IFN-λ signaling accelerates autoimmunity development and promotes systemic and renal inflammation.
- Blocking type III interferon receptor signaling offers a potential therapeutic avenue for managing lupus and related autoimmune conditions.
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