Thread by @TuckerGoodrich

"...structural changes in the LDL particle upon its mild oxidation make it also recognizable by immune competent cells and lead to TLR4 activation."

"These data and other results from our group support the hypothesis of convergence of immune responses to oxidation-specific self-antigens and to microbial infection."

"This hypothesis was first substantiated by data from our group showing that a natural autoantibody to mmLDL, EO6, is genetically identical to the classic germline anti-phosphorylcholine antibody T15, which binds avidly to Streptococcus pneumoniae."

"More specifically, EO6/T15 recognize bacterial cell wall polysaccharides that are rich in phosphorylcholine (57), as well as phosphorylcholine-containing oxidized phospholipids present in oxidized LDL (22) and cells undergoing apoptosis (23)."

"The present study demonstrates correspondence not only in humoral (EO6-T15 antibody) but also in cellular (CD14 and TLR4 receptors) immune responses to mmLDL and to microbial infection."

"The exact mechanisms by which macrophages exposed to mmLDL (or M-CSF) become less efficient phagocytes but have a higher rate of OxLDL uptake are not yet known."

"Thus, this study defines novel pathways by which both mmLDL and microbial infection could influence the progress of atherogenesis."

"Minimally Modified LDL Binds to CD14, Induces Macrophage Spreading via TLR4/MD-2, and Inhibits Phagocytosis of Apoptotic Cells"

m.jbc.org/content/278/3/…

#lcl6 OxLDL