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IL-23R deficiency d...
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Engelbertsen, DanielLund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups,Brigham and Women's Hospital / Harvard Medical School,Harvard University
(author)
IL-23R deficiency does not impact atherosclerotic plaque development in mice
- Article/chapterEnglish2018
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LIBRIS-ID:oai:lup.lub.lu.se:afafc91c-d3b3-4e96-9030-8ccae0c7310f
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https://lup.lub.lu.se/record/afafc91c-d3b3-4e96-9030-8ccae0c7310fURI
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https://doi.org/10.1161/JAHA.117.008257DOI
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Language:English
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Summary in:English
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Background--Interleukin-23 (IL-23) has been implicated in inflammatory and autoimmune diseases by skewing CD4+ T helper cells towards a pathogenic Th17 phenotype. In this study we investigated the presence of IL-23 receptor (IL-23R)-expressing cells in the atherosclerotic aorta and evaluated the effect of IL-23R deficiency on atherosclerosis development in mice. Methods and Results--We used heterozygous Ldlr-/-Il23reGFP/WT knock-in mice to identify IL-23R-expressing cells by flow cytometry and homozygous Ldlr-/-Il23reGFP/eGFP (Ldlr-/- Il23r-/-) mice to investigate the effect of lack of IL-23R in atherosclerosis. We demonstrate the presence of relatively rare IL-23R-expressing cells in lymphoid tissue and aorta (≈0.1-1% IL23R+ cells of all CD45+ leukocytes). After 10 weeks on a high-fat diet, production of IL-17, but not interferon-c, by CD4+ T cells and other lymphocytes was reduced in Ldlr-/- Il23r-/- compared with Ldlr-/-controls. However, Ldlr-/- and Ldlr-/-Il23r-/- mice had equivalent amounts of aortic sinus and descending aorta lesions. Adoptive transfer of IL-23R-deficient CD4+ T cells to lymphopenic Ldlr-/-Rag1-/- resulted in dramatically reduced IL-17-producing T cells but did not reduce atherosclerosis, compared with transfer of IL-23R-sufficient CD4+ T cells. Conclusions--These data demonstrate that loss of IL-23R does not affect development of experimental atherosclerosis in LDLrdeficient mice, despite a role for IL-23 in differentiation of IL-17-producing T cells.
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Depuydt, Marie A.C.Harvard University,Brigham and Women's Hospital / Harvard Medical School
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Verwilligen, Robin A.F.Harvard University,Brigham and Women's Hospital / Harvard Medical School
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Rattik, SaraLund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups(Swepub:lu)med-srk
(author)
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Levinsohn, ErikHarvard University,Brigham and Women's Hospital / Harvard Medical School
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Edsfeldt, AndreasLund University,Lunds universitet,Kardiovaskulär forskning - immunitet och ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Immunity and Atherosclerosis,Lund University Research Groups(Swepub:lu)med-aet
(author)
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Kuperwaser, FeliciaBrigham and Women's Hospital / Harvard Medical School,Harvard University
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Jarolim, PetrHarvard University,Brigham and Women's Hospital / Harvard Medical School
(author)
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Lichtman, Andrew H.Brigham and Women's Hospital / Harvard Medical School,Harvard University
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Kardiovaskulär forskning - immunitet och aterosklerosForskargrupper vid Lunds universitet
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In:Journal of the American Heart Association7:82047-9980
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