Promise of immune modulation to inhibit atherogenesis.

t is now widely recognized that the evolving atherosclerotic esion has nearly all of the characteristics of a chronic nflammatory disease, including the active participation of any arcs of immune function. That immune mechanisms lay an important, if not dominant, role once atherosclerosis as been initiated is attested to by scores of examples in hich manipulations of both adaptive and innate immune unction have profoundly impacted atherogenesis in murine odels, accelerating it or providing atheroprotective influnces (1–5).