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  Vol. 159 No. 3, February 8, 1999 TABLE OF CONTENTS
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  •  Online Features
  Editor's Correspondence
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Atherosclerosis and the Immune System

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The recently published study by Kovanen et al1 and the editorial accompanying the study2 reopen an important question for the area of clinical and fundamental research concerning the role of inflammatory events in the initiation and progression of the atherosclerotic lesion. Despite the clinical and experimental data accumulated during the last 2 decades, the importance of the inflammatory events in atherogenesis is still underestimated.

Several pieces of information could be added to the data presented in the above-mentioned articles.1-2 The role of the complement system in the pathogenesis of atherosclerosis has been documented by clinical and experimental studies. The complement system, a complex of enzymes and regulators, has multiple biological effects in circulation and in tissues inducing opsonization, chemoattraction of leukocytes, cell lysis, and cell activation and rescue from apoptosis.3 In previous studies we have demonstrated a complex relationship between the circulating immunoglobulins deposited as immune complexes in the arterial . . . [Full Text of this Article]


RELATED LETTER

Immunoglobulins, C3, and the Risk of Myocardial Infarction
Antonio Muscari, Paolo Puddu, Petri T. Kovanen, Matti Mänttäri, Timo Palosuo, Vesa Manninen, and Kimmo Aho
Arch Intern Med. 1999;159(19):2364-2365.
EXTRACT | FULL TEXT  


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Systemic lupus erythematosus: a model for atherogenesis?
Manzi
Rheumatology (Oxford) 2000;39:353-359.
FULL TEXT  

Immunoglobulins, C3, and the Risk of Myocardial Infarction
Muscari et al.
Arch Intern Med 1999;159:2364-2365.
FULL TEXT  





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