Does toll-like receptor 3 and 4 signalling through the TRIF and TRAM adaptors in haematopoietic cells promote atherosclerosis?
By studying hypercholesterolaemic mice with defects in TLR-signalling adaptors, we demonstrated that deleting either TRAM or TRIF in immune cells is sufficient to attenuate vessel inflammation and protect against atherosclerosis. In addition, these adaptors elicit partly different sets of inflammatory mediators and can independently inhibit the disease process. Furthermore, we identify TLR3 as a pro-atherogenic receptor in haematopoietic immune cells. The identification of these pro-atherogenic pathways downstream of TLR3 and TLR4 contributes to a better understanding of TLRs and their signalling pathways in the pathogenesis of atherosclerosis.
Overexpression of the LMW-cyclin E or total cyclin E is a strong predictor for poorer survival in patients with rectal cancer. Therefore, evaluating cyclin E expression may provide useful prognostic information for resectable rectal cancer patients.