Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Early Treatment of Interleukin-33 Can Attenuate Lupus Development in Young NZB/W F1 Mice

Version 1 : Received: 8 October 2020 / Approved: 12 October 2020 / Online: 12 October 2020 (14:59:30 CEST)

How to cite: Mohd Jaya, F.N.; Liu, Z.; Chan, G.C. Early Treatment of Interleukin-33 Can Attenuate Lupus Development in Young NZB/W F1 Mice. Preprints 2020, 2020100246 (doi: 10.20944/preprints202010.0246.v1). Mohd Jaya, F.N.; Liu, Z.; Chan, G.C. Early Treatment of Interleukin-33 Can Attenuate Lupus Development in Young NZB/W F1 Mice. Preprints 2020, 2020100246 (doi: 10.20944/preprints202010.0246.v1).

Abstract

Interleukin-33 (IL-33), a member of the IL-1 cytokine family has been recently associated with the development of autoimmune diseases, including SLE. IL-33 is an alarmin and a pleiotropic cytokine that affects various types of immune cells via binding to its receptor, ST2. In this study, we determine the impact of intraperitoneal IL-33 treatments in young lupus, NZB/W F1 mice. Mice were treated from the age of 6 to 11 weeks. We then assessed the proteinuria level, renal damage, survival rate, and anti-dsDNA antibodies. The induction of regulatory B (Breg) cells and changes in gene expression were also examined. In comparison to the control group, young NZB/W F1 mice administered with IL-33 had a better survival rate as well as reduced proteinuria level and lupus nephritis. IL-33 treatments significantly induced IgM anti-dsDNA antibody, IL-10 expressing Breg cells, and alternatively induced M2 macrophage gene signatures. These results imply that IL-33 exhibit regulatory roles during lupus onset via the expansion of protective IgM anti-dsDNA as well as regulatory cells such as Bregs and M2 macrophages.

Subject Areas

Interleukin-33; Cytokine; Systemic Lupus Erythematosus; Regulatory B cells; autoimmune disease

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