Affordable Access

Access to the full text

ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions

Authors
  • Mantani, Polyxeni T.1, 2
  • Dunér, Pontus1, 2
  • Ljungcrantz, Irena1, 2
  • Nilsson, Jan1, 2
  • Björkbacka, Harry1, 2
  • Fredrikson, Gunilla Nordin1, 2
  • 1 Skåne University Hospital Malmö, CRC, Building 91:12, Jan Waldenströms gata 35, Malmö, 20502, Sweden , Malmö (Sweden)
  • 2 Lund University, Lund, Sweden , Lund (Sweden)
Type
Published Article
Journal
BMC Immunology
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Dec 10, 2019
Volume
20
Issue
1
Identifiers
DOI: 10.1186/s12865-019-0330-z
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundExpansion 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.ResultsImmunomagnetically 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.ConclusionsWith 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.

Report this publication

Statistics

Seen <100 times