Atherosclerosis is a chronic, inflammatory disease driven by the continuous emigration of monocytes into the vessel wall. CD40L is an established marker and mediator of chronic inflammatory diseases such as atherosclerosis. While anti-CD40L treatment generated promising results in clinical trials, elevated thrombembolic complications prohibited the pursuit of this strategy. Baker IDI researchers previously reported that CD40L mediates atherogenesis independently of CD40 in mice, proposing a novel interaction with the leukocyte integrin Mac-1. Targeting of CD40L/Mac-1 binding with an inhibitory peptide, cM7, proofed to be specific and ultimately effective in attenuating inflammation and atherosclerotic lesion formation in mice. Specific inhibition of the CD40L/Mac-1 dyad therefore represents an attractive novel anti-inflammatory treatment strategy for atherosclerosis and other chronic inflammatory diseases, promising minimal side effects.
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