NSG Mice Lacking Apoe: An Immunodeficient Mouse Model of Atherosclerosis.
- 1The Jackson Laboratory, Bar Harbor, Maine, USA.
- 2Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, Maine, USA.
- 3Program in Molecular Medicine, Diabetes Center of Excellence, UMass Chan Medical School, Worcester, Massachusetts, USA.
Abstract
Murine research on atherosclerosis has been conducted largely on the C57BL/6 (B6) strain background, and most commonly, the B6.129P2-Apoetm1Unc/J (B6-ApoEKO) strain. The use of the B6 background strain limits translatability for immunotherapy development due to inherent species differences between human and mouse immune systems. A proposed solution to this limitation is a humanized mouse model of atherosclerosis that would support the engraftment of human lymphoid and myeloid cell populations. The development of such a model has been hindered by the lack of a mouse strain that both develops atherosclerosis and supports human immune cell engraftment. In this paper, we report on a NOD.Cg-PrkdcscidIl2rgtm1Wjl/Sz (NSG) immunodeficient mouse strain that has a 383 bp deletion in the Apoe gene which prevents ApoE protein expression. When maintained on a high fat diet, NSG-ApoEKO mice develop hypercholesteremia and atherosclerosis at levels similar to B6-ApoEKO mice. While atherosclerosis in B6-ApoEKO mice has been widely studied in many laboratories under multiple conditions, our initial study of disease development in NSG-ApoEKO mice was limited and future comparative studies with B6-ApoEKO mice are necessary. NSG-ApoEKO mice concomitantly support human cell engraftment while developing atherosclerosis, thereby making them useful to study human-specific immune aspects.
Related
- IRE1 deficiency in myeloid cells increases atherosclerosis in apoE−/− mice
- Differential Effects of Direct Plasmin Inhibition and Tranexamic Acid on Atherosclerosis Progression and Vascular Remodeling in Apoe/Ldlr Double-Knockout Mice
- Resmetirom attenuates atherosclerosis-associated dyslipidemia and vascular inflammation in high-fat diet-fed ApoE⁻/⁻ mice
- Smooth muscle cell mineralocorticoid receptor does not contribute to atherosclerosis in male or female ApoE-knockout mice
- Functional Humanization of Mouse Alox15 Does Not Alter Early Vascular Lipid Deposition in ApoE-Deficient Mice
BibTeX
@article{megathlin2026mice,
title = {{NSG Mice Lacking Apoe: An Immunodeficient Mouse Model of Atherosclerosis.}},
author = {Hannah R Megathlin and Lisa Burzenski and David A Coleman and Blaze Albert and Michelle L Farley and Michael A Brehm and Dale L Greiner and Leonard D Shultz},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
year = {2026},
month = oct,
doi = {10.1096/fj.202603399r},
url = {https://europepmc.org/article/MED/42905940},
note = {CC BY},
}
RIS
TY - JOUR
TI - NSG Mice Lacking Apoe: An Immunodeficient Mouse Model of Atherosclerosis.
AU - Hannah R Megathlin
AU - Lisa Burzenski
AU - David A Coleman
AU - Blaze Albert
AU - Michelle L Farley
AU - Michael A Brehm
AU - Dale L Greiner
AU - Leonard D Shultz
PY - 2026
DA - 2026/10/01
JO - FASEB journal : official publication of the Federation of American Societies for Experimental Biology
DO - 10.1096/fj.202603399r
UR - https://europepmc.org/article/MED/42905940
AB - Murine research on atherosclerosis has been conducted largely on the C57BL/6 (B6) strain background, and most commonly, the B6.129P2-Apoetm1Unc/J (B6-ApoEKO) strain. The use of the B6 background strain limits translatability for immunotherapy development due to inherent species differences between human and mouse immune systems. A proposed solution to this limitation is a humanized mouse model of atherosclerosis that would support the engraftment of human lymphoid and myeloid cell populations. The development of such a model has been hindered by the lack of a mouse strain that both develops atherosclerosis and supports human immune cell engraftment. In this paper, we report on a NOD.Cg-PrkdcscidIl2rgtm1Wjl/Sz (NSG) immunodeficient mouse strain that has a 383 bp deletion in the Apoe gene which prevents ApoE protein expression. When maintained on a high fat diet, NSG-ApoEKO mice develop hypercholesteremia and atherosclerosis at levels similar to B6-ApoEKO mice. While atherosclerosis in B6-ApoEKO mice has been widely studied in many laboratories under multiple conditions, our initial study of disease development in NSG-ApoEKO mice was limited and future comparative studies with B6-ApoEKO mice are necessary. NSG-ApoEKO mice concomitantly support human cell engraftment while developing atherosclerosis, thereby making them useful to study human-specific immune aspects.
SN - 0892-6638
SN - 1530-6860
ER -