Key result
Siglec-G deficiency reduces plaque formation and hepatic inflammation via increased protective IgM against OxLDL.
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Atherosclerosis is initiated and sustained by hypercholesterolemia, which results in the generation of oxidized LDL (OxLDL) and other metabolic byproducts that trigger inflammation. Specific immune responses have been shown to modulate the inflammatory response during atherogenesis. The sialic acid-binding immunoglobulin-like lectin G (Siglec-G) is a negative regulator of the functions of several immune cells, including myeloid cells and B-1 cells. Here, we show that deficiency of Siglec-G in atherosclerosis-prone mice inhibits plaque formation and diet-induced hepatic inflammation. We further demonstrate that selective deficiency of Siglec-G in B cells alone is sufficient to mediate these effects. Levels of B-1 cell-derived natural IgM with specificity for OxLDL were significantly increased in the plasma and peritoneal cavity of Siglec-G-deficient mice. Consistent with the neutralizing functions of OxLDL-specific IgM, Siglec-G-deficient mice were protected from OxLDL-induced sterile inflammation. Thus, Siglec-G promotes atherosclerosis and hepatic inflammation by suppressing protective anti-inflammatory effector functions of B cells.
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Gruber et al. (2016) studied Atherosclerosis and hepatic inflammation. Siglec-G deficiency vs. Siglec-G sufficient atherosclerosis-prone mice was evaluated on Atherosclerotic plaque formation and diet-induced hepatic inflammation. Siglec-G deficiency in atherosclerosis-prone mice inhibited plaque formation and diet-induced hepatic inflammation while significantly increasing B-1 cell-derived natural IgM specific for OxLDL.
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