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Volume 176, Issue 1, Pages 101-110 (September 2004)


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Emergence of dendritic cells in rupture-prone regions of vulnerable carotid plaques

Atilla YilmazaCorresponding Author Informationemail address, Marlene Lochnoa, Friedemann Traega, Iwona Cichaa, Christine Reissa, Christian Stumpfa, Dorette Raaza, Thomas Angera, Kerstin Amannb, Thomas Probstc, Josef Ludwiga, Werner G Daniela, Christoph D Garlichsa

Received 19 December 2003; received in revised form 25 March 2004; accepted 20 April 2004.

Abstract 

Dendritic cells (DC), which are critically involved in various immunological disorders, were detected in atherosclerotic plaques in 1995. Since DC might be related to the immunological processes in atherosclerosis (AS), we analyzed the emergence of DC and other inflammatory cells in different stages of AS. Serial cross-sections of 44 carotid specimens were immunohistochemically analyzed for the presence of DC, T cells, macrophages, and HLA-DR. Atherosclerotic specimens were histologically defined as initial lesions, advanced stable, or vulnerable plaques. In initial lesions significantly lower DC numbers were detected than in advanced plaques (P < 0.001). For advanced plaques, DC numbers were significantly higher in vulnerable than in stable plaques (P = 0.005). In contrast to initial lesions, approximately 70% of DC in advanced plaques exhibited a mature phenotype (CD83+, DC-LAMP+), indicating a functional activity of DC. In plaques of patients with acute ischemic symptoms DC numbers were markedly elevated (P = 0.03), whereas significantly lower DC numbers and more often a stable plaque morphology were detected in statin-treated patients (P = 0.02). DC clusters with a strong HLA-DR expression and frequent DC-T cell contacts were located particularly in the rupture-prone plaque regions and at complications. The results of the present study indicate that DC might contribute to plaque destabilization through an activation of T cells.

a Medical Clinic II, University of Erlangen-Nuremberg, Ulmenweg 18, 91054 Erlangen, Germany

b Department of Pathology, University of Erlangen-Nuremberg, Hartmannstraβe 4, 91052 Erlangen, Germany

c Department of Vascular Surgery, Clinic Nuremberg, Breslauer Straβe 201, 90340 Nuremberg, Germany

Corresponding Author InformationCorresponding author. Tel.: +49 9131 853 5301; fax: +49 9131 853 2079.

PII: S0021-9150(04)00217-5

doi:10.1016/j.atherosclerosis.2004.04.027


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