Therefore, it seemed likely that scavenger receptors may be involved in the uptake of cholesteryl esters, especially SR-BI.
These observations suggested that scavenger receptors modulate inflammation without altering ox-LDL accumulation in the liver.
It is known that scavenger receptors belong to the large family of signaling pattern-recognition receptors or PRRs [ 6].
This is, potentially, a highly significant area of Cryptococcus research but there are still fundamental gaps in our understanding, for example, a direct demonstration that scavenger receptors mediate the uptake of cryptococci in vivo.
Similarly, we showed that scavenger receptor-A (SR-A), 'macrophage associated receptor with a collagenous base' (MARCO), CD36, or TLR2 deficiency protect mice against peritoneal S. aureus infection while these deficiencies aggravated pneumonia [ 62].
LG will react with these molecules 3 orders of magnitude faster than lysine, and we have previously shown that scavenger treatment decreases total cellular levels of LG-lysine adducts without affecting PGE2 production.
