| First Author | Martin P | Year | 2015 |
| Journal | Immun Inflamm Dis | Volume | 3 |
| Issue | 3 | Pages | 239-46 |
| PubMed ID | 26417439 | Mgi Jnum | J:250083 |
| Mgi Id | MGI:6102221 | Doi | 10.1002/iid3.62 |
| Citation | Martin P, et al. (2015) Atherosclerosis severity is not affected by a deficiency in IL-33/ST2 signaling. Immun Inflamm Dis 3(3):239-46 |
| abstractText | Interleukin (IL)-33 is a cytokine of the IL-1 family, which signals through the ST2 receptor. Previous work demonstrated that the systemic administration of recombinant IL-33 reduces the development of atherosclerosis in apolipoprotein E-deficient (ApoE(-/-)) mice by inducing a Th1-to-Th2 shift. The objective of our study was to examine the role of endogenous IL-33 and ST2 in atherosclerosis. ApoE(-/-), IL-33(-/-)ApoE(-/-), and ST2(-/-)ApoE(-/-) mice were fed with a cholesterol-rich diet for 10 weeks. Additionally, a group of ApoE(-/-) mice was injected with a neutralizing anti-ST2 or an isotype control antibody during the period of the cholesterol-rich diet. Atherosclerotic lesion development was measured by Oil Red O staining in the thoracic-abdominal aorta and the aortic sinus. There were no significant differences in the lipid-staining area of IL-33(-/-)ApoE(-/-), ST2(-/-)ApoE(-/-), or anti-ST2 antibody-treated ApoE(-/-) mice, compared to ApoE(-/-) controls. The absence of IL-33 signaling had no major and consistent impact on the Th1/Th2 cytokine responses in the supernatant of in vitro-stimulated lymph node cells. In summary, deficiency of the endogenously produced IL-33 and its receptor ST2 does not impact the development of atherosclerosis in ApoE-deficient mice. |
