IL-25 Inhibits Atherosclerosis Development in Apolipoprotein E Deficient Mice

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IL-25 Inhibits Atherosclerosis Development in Apolipoprotein E Deficient Mice

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Publication Article, peer reviewed scientific
Title IL-25 Inhibits Atherosclerosis Development in Apolipoprotein E Deficient Mice
Author(s) Mantani, Polyxeni T. ; Duner, Pontus ; Bengtsson, Eva ; Alm, Ragnar ; Ljungcrantz, Irena ; Soderberg, Ingrid ; Sundius, Lena ; To, Fong ; Nilsson, Jan ; Bjorkbacka, Harry ; Fredrikson, Gunilla Nordin
Date 2015
English abstract
Objective IL-25 has been implicated in the initiation of type 2 immunity and in the protection against autoimmune inflammatory diseases. Recent studies have identified the novel innate lymphoid type 2 cells (ILC2s) as an IL-25 target cell population. The purpose of this study was to evaluate if IL-25 has any influence on atherosclerosis development in mice. Methods and Results Administration of 1 mu g IL-25 per day for one week to atherosclerosis-prone apolipoprotein (apo) E deficient mice, had limited effect on the frequency of T cell populations, but resulted in a large expansion of ILC2s in the spleen. The expansion was accompanied by increased levels of anti-phosphorylcholine (PC) natural IgM antibodies in plasma and elevated levels of IL-5 in plasma and spleen. Transfer of ILC2s to apoE deficient mice elevated the natural antibody-producing B1a cell population in the spleen. Treatment of apoE/Rag-1 deficient mice with IL-25 was also associated with extensive expansion of splenic ILC2s and increased plasma IL-5, suggesting ILC2s to be the source of IL-5. Administration of IL-25 in IL-5 deficient mice resulted in an expanded ILC2 population, but did not stimulate generation of anti-PC IgM, indicating that IL-5 is not required for ILC2 expansion but for the downstream production of natural antibodies. Additionally, administration of 1 mu g IL-25 per day for 4 weeks in apoE deficient mice reduced atherosclerosis in the aorta both during initiation and progression of the disease. Conclusions The present findings demonstrate that IL-25 has a protective role in atherosclerosis mediated by innate responses, including ILC2 expansion, increased IL-5 secretion, B1a expansion and natural anti-PC IgM generation, rather than adaptive Th2 responses.
DOI (link to publisher's fulltext)
Publisher Public Library of Science
Host/Issue PLoS One;1
Volume 10
ISSN 1932-6203
Pages e0117255
Language eng (iso)
Subject(s) Spleen
Flow cytometry
Cell staining
Immune response
Research Subject Categories::MEDICINE
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