| First Author | Tsiantoulas D | Year | 2017 |
| Journal | Circ Res | Volume | 120 |
| Issue | 1 | Pages | 78-84 |
| PubMed ID | 27903567 | Mgi Jnum | J:262028 |
| Mgi Id | MGI:6156704 | Doi | 10.1161/CIRCRESAHA.116.309606 |
| Citation | Tsiantoulas D, et al. (2017) Increased Plasma IgE Accelerate Atherosclerosis in Secreted IgM Deficiency. Circ Res 120(1):78-84 |
| abstractText | RATIONALE: Deficiency of secreted IgM (sIgM(-/-)) accelerates atherosclerosis in Ldlr(-/-)mice. Several atheroprotective effects of increased levels of IgM antibodies have been suggested, including preventing inflammation induced by oxidized low-density lipoprotein and promoting apoptotic cell clearance. However, the mechanisms by which the lack of sIgM promotes lesion formation remain unknown. OBJECTIVE: To identify the mechanisms by which sIgM deficiency accelerates atherosclerosis in mice. METHODS AND RESULTS: We here show that both sIgM(-/-) and Ldlr(-/-)sIgM(-/-) mice develop increased plasma IgE titers because of impaired generation of B cells expressing the low-affinity IgE receptor CD23, which mediates the clearance of IgE antibodies. We further report that Ldlr(-/-)sIgM(-/-) mice exhibit increased numbers of activated mast cells and neutrophils in the perivascular area of atherosclerotic plaques. Treatment with an anti-IgE-neutralizing antibody fully reversed vascular inflammation and accelerated atherosclerotic lesion formation in cholesterol-fed Ldlr(-/-)sIgM(-/-) mice. CONCLUSIONS: Thus, our data identify a previously unsuspected mechanism by which sIgM deficiency aggravates atherosclerosis. |
