ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions
Abstract Background Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) and killer-cell lectin like receptor G1 (...
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doaj-f4aaddf2ec704a479c423beb414e3eef2020-12-13T12:41:37ZengBMCBMC Immunology1471-21722019-12-0120111310.1186/s12865-019-0330-zILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesionsPolyxeni T. Mantani0Pontus Dunér1Irena Ljungcrantz2Jan Nilsson3Harry Björkbacka4Gunilla Nordin Fredrikson5Department of Clinical Sciences, Skåne University Hospital MalmöDepartment of Clinical Sciences, Skåne University Hospital MalmöDepartment of Clinical Sciences, Skåne University Hospital MalmöDepartment of Clinical Sciences, Skåne University Hospital MalmöDepartment of Clinical Sciences, Skåne University Hospital MalmöDepartment of Clinical Sciences, Skåne University Hospital MalmöAbstract Background Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) and killer-cell lectin like receptor G1 (KLRG1) expression. The aim of the current study is to characterize the interleukin 25 (IL25)-induced splenic ILC2 population (Lin−CD45+IL17RB+ICOS+IL7raintermediate) and address its direct role in experimental atherosclerosis by its adoptive transfer to hypercholesterolaemic apolipoprotein E deficient (apoE−/−) mice. Results Immunomagnetically enriched, FACS-sorted ILC2s from the spleens of IL-25 treated apoE−/− mice were stained for KLRG1 and ST2 directly upon cell obtainment or in vitro cell expansion for flow cytometric analysis. IL25-induced splenic ILC2s express high levels of both KLRG1 and ST2. However, both markers are downregulated upon in vitro cell expansion. In vitro expanded splenic ILC2s were intraperitoneally transferred to apoE−/− recipients on high fat diet. ApoE−/− mice that received in vitro expanded splenic ILC2s had decreased lipid content in subvalvular heart and brachiocephalic artery (BCA) plaques accompanied by increased peritoneal B1 cells, activated eosinophils and alternatively activated macrophages (AAMs) as well as anti-phosphorylcholine (PC) immunoglobulin (Ig) M in plasma. Conclusions With the current data we designate the IL25-induced ILC2 population to decrease the lipid content of atherosclerotic lesions in apoE−/− mice and we directly link the induction of B1 cells and the atheroprotective anti-PC IgM antibodies with ILC2s.https://doi.org/10.1186/s12865-019-0330-zILC2sIL-25Apolipoprotein E deficient miceB1 cellsAnti-PC IgMEosinophils |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Polyxeni T. Mantani Pontus Dunér Irena Ljungcrantz Jan Nilsson Harry Björkbacka Gunilla Nordin Fredrikson |
spellingShingle |
Polyxeni T. Mantani Pontus Dunér Irena Ljungcrantz Jan Nilsson Harry Björkbacka Gunilla Nordin Fredrikson ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions BMC Immunology ILC2s IL-25 Apolipoprotein E deficient mice B1 cells Anti-PC IgM Eosinophils |
author_facet |
Polyxeni T. Mantani Pontus Dunér Irena Ljungcrantz Jan Nilsson Harry Björkbacka Gunilla Nordin Fredrikson |
author_sort |
Polyxeni T. Mantani |
title |
ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions |
title_short |
ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions |
title_full |
ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions |
title_fullStr |
ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions |
title_full_unstemmed |
ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions |
title_sort |
ilc2 transfers to apolipoprotein e deficient mice reduce the lipid content of atherosclerotic lesions |
publisher |
BMC |
series |
BMC Immunology |
issn |
1471-2172 |
publishDate |
2019-12-01 |
description |
Abstract Background Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) and killer-cell lectin like receptor G1 (KLRG1) expression. The aim of the current study is to characterize the interleukin 25 (IL25)-induced splenic ILC2 population (Lin−CD45+IL17RB+ICOS+IL7raintermediate) and address its direct role in experimental atherosclerosis by its adoptive transfer to hypercholesterolaemic apolipoprotein E deficient (apoE−/−) mice. Results Immunomagnetically enriched, FACS-sorted ILC2s from the spleens of IL-25 treated apoE−/− mice were stained for KLRG1 and ST2 directly upon cell obtainment or in vitro cell expansion for flow cytometric analysis. IL25-induced splenic ILC2s express high levels of both KLRG1 and ST2. However, both markers are downregulated upon in vitro cell expansion. In vitro expanded splenic ILC2s were intraperitoneally transferred to apoE−/− recipients on high fat diet. ApoE−/− mice that received in vitro expanded splenic ILC2s had decreased lipid content in subvalvular heart and brachiocephalic artery (BCA) plaques accompanied by increased peritoneal B1 cells, activated eosinophils and alternatively activated macrophages (AAMs) as well as anti-phosphorylcholine (PC) immunoglobulin (Ig) M in plasma. Conclusions With the current data we designate the IL25-induced ILC2 population to decrease the lipid content of atherosclerotic lesions in apoE−/− mice and we directly link the induction of B1 cells and the atheroprotective anti-PC IgM antibodies with ILC2s. |
topic |
ILC2s IL-25 Apolipoprotein E deficient mice B1 cells Anti-PC IgM Eosinophils |
url |
https://doi.org/10.1186/s12865-019-0330-z |
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