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To the Editor: Accumulating evidence suggests a predictive role of elevated serum concentrations of C-reactive protein (CRP) for atherosclerosis and its thrombotic complications.1 These findings apparently reflect an inflammatory component of the multifactorial atherosclerotic process. Furthermore, it is increasingly recognized that CRP may not merely represent an indicator of inflammation but may also, because of its known functional properties, be actively involved in the initiation or perpetuation of local inflammatory reactions.2 3 A direct approach in the study of the latter hypothesis is the search for CRP in atherosclerotic lesions. [banner]In this context, the recent publication of Torzewski et al4 in Arteriosclerosis, Thrombosis, and Vascular Biology is of actual relevance. By means of immunohistochemistry, the authors clearly demonstrate deposits of CRP beside terminal complement proteins in the arterial wall of patients with early atherosclerotic lesions. Because ligand-bound CRP activates the classical pathway of complement, the authors suggest that the colocalization of terminal complement proteins with CRP might reflect complement activation by CRP in situ. Even if we share the hypothesis that …

Deposition of Modified or Native C-Reactive Protein in Atherosclerotic Arteries?