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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1173.)
© 2000 American Heart Association, Inc.

Letters to the Editor

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

Peter Vaith

Abteilung Rheumatologie und Klinische Immunologie, Medizinische Unversitätsklinik, Universitäts Freiburg Klinikum, Freiburg, Germany

Lawrence A. Potempa

Next Era Therapeutics, Inc, Vernon Hills, Illinois

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 CRP may contribute to local complement activation, this conclusion is not unequivocally supported by the presented findings. The monoclonal antibody against CRP used in that study (clone CRP-8 from Sigma) exclusively recognizes a modified form of CRP (mCRP) and not the native CRP molecule. This restricted specificity of clone CRP-8 against mCRP described by the manufacturer (Sigma) was recently confirmed experimentally by us.⁵ Differentiating between both CRP variants may be functionally relevant, because mCRP, contrary to its native counterpart, . . . [Full Text of this Article]

Jan Torzewski, MD, MPhil

Department of Cardiology, Internal Medicine II, University of Ulm, Ulm, Germany

Michael Torzewski, MD

Department of Clinical Chemistry, University of Regensburg, Regensburg, Germany