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Atherosclerosis can be seen as a dynamic chronic inflammatory process, in which flares of inflammatory and thrombotic activity underlie the clinical presentations of unstable angina and myocardial infarction.1 ,2 In this issue ofHeart, two articles draw attention to the inflammatory basis of acute coronary syndromes (ACS).
More evidence for circulating activated leucocytes
The first study, by Hillis and colleagues,3focuses on expression and function of the β2 integrin CD11b/CD18 (Mac-1, CR3). The β2 integrins are a family of four heterodimers, in which separate α chains (CD11a–d) combine with a common β chain (CD18). CD11b/CD18 (Mac-1, CR3) is critical for leucocyte adhesion and migration, and also acts as a receptor for complement C3bi. In addition, CD11b/CD18 is a signalling molecule and is necessary for many other neutrophil and monocyte effector functions in inflammation.4 Both neutrophils and monocytes normally carry CD11b/CD18 on the cell surface, and also contain additional stores of the heterodimer in the membranes of intracellular granules. Translocation of granules to the cell surface upon cell activation therefore results in increased adhesion potential. Importantly, however, the adhesion function of CD11b/CD18 depends more on affinity and avidity changes than on the absolute level of expression, and these are thought to involve signalling events within the surface membrane and cytoskeleton and the binding of divalent cations. Despite this qualification, increased surface expression of CD11b/CD18 is commonly associated with increased adhesive function, and hence measuring CD11b/CD18 expression in clinical samples may provide useful indirect information.
Hillis and colleagues found increased expression of CD11b/CD18 on circulating neutrophils and monocytes of patients with unstable angina, and although the numbers were small, this …