Ozlem Equils

TL;DR: This study demonstrates that TLR-4 is preferentially expressed by macrophages in murine and human lipid-rich atherosclerotic lesions, where it may play a role to enhance and sustain the innate immune and inflammatory responses.

TL;DR: It is shown that human dermal microvessel endothelial cells (HMEC) and human umbilical vein endothelial Cells express predominantly TLR-4 but very weakTLR-2 and respond vigorously to LPS but not to Mycobacterium tuberculosis 19-kDa lipoprotein.

TL;DR: It is reported that human dermal endothelial cells (HMEC) are unresponsive to several additional biologically relevant TLR2 ligands, including, phenol-soluble modulin (PSM), a complex of three small secreted polypeptides from the skin commensal Staphylococcus epidermidis, soluble tuberculosis factor (STF), and Borrelia burgdorferi outer surface protein A lipoprotein (OspA-L).

TL;DR: It is shown that LPS, TNF-α, or IFN-γ induce TLR2 expression in both human dermal microvessel EC and HUVEC, and LPS-induced TLR 2 expression is NF-κB dependent and TLR4 mRNA expression in EC is up-regulate.

TL;DR: Results indicate that cHSP60 is a potent inducer of vascular EC and macrophage inflammatory responses, which are very relevant to atherogenesis.