Anh Thu Gaston

TL;DR: The study suggests that interventional tools able to revert the MØ infiltrate towards the M2 phenotype may exert an atheroprotective action.

TL;DR: It is concluded that the loss of T cell regulation caused by CD31 shedding driven by TCR stimulation can be rescued by molecular tools able to engage the truncated juxta-membrane extracellular molecule that remains exposed at the surface of CD31shed cells.

TL;DR: These results are the first to identify M1 macrophages as inducer cells that trigger the expression of chemokines by VSMCs independently of LTβR signalling.

TL;DR: It is shown that CD31 is a key coinhibitory receptor on stimulated DCs, favoring the development of tolerogenic functions and finally resulting in T-cell tolerance, which has important implications both in settings where the immunogenic function of DCs is desirable, such as infection and cancer, and in settingsWhere tolerance-driving DCs are preferred.

TL;DR: CD31 peptides could represent a new class of drugs intended to prevent the inflammatory cell processes, such as those underlying progression of atherosclerosis and development of AAA, in patients and mice.