A hypothetical model for the role of a newly described receptor for phosphatidylserine (PS) (26) in modulating inflammation and immune response. Engulfment of microbial organisms that fail to express PS externally does not engage the PS receptor (PSR); instead, receptors are stimulated by the microbe or its products that transduce proinflammatory signals. These include receptors for immunoglobulin, complement, collectins, endotoxin, etc. In contrast, when apoptotic cells are recognized, they expose PS, thus engaging the PSR, which provides an anti-inflammatory signal. TLR, toll-like receptor.