Pentraxins, Anti-pentraxin Antibodies, and Atherosclerosis N. Bassi & S. Zampieri & A. Ghirardello & M. Tonon & M. Zen & F. Cozzi & A. Doria Published online: 18 November 2008 # Humana Press Inc. 2008 Abstract Atherosclerosis is a disease of the vascular wall, which predominantly affects large and medium-sized arteries. It represents a leading cause of morbidity and mortality in the Western world. In the last few decades, it has been clearly shown that immune system plays a relevant role in atherogenesis. The effectors of both innate and adaptive immunity, including immune cells, cell or soluble receptors, cytokines, chemokines, complement com- ponents or coagulation systems, and autoantibodies are able to modulate atherosclerosis. Among proteins belonging to innate immunity, the highly conserved pentraxin family, which encompass C-reactive protein (CRP), serum amyloid P (SAP), and the long pentraxin 3 (PTX3) seems to be directly involved in the induction and progression of atherosclerosis. By immunohistochemical staining, pentraxins were found within the atherosclerotic plaques where they could play a key role interacting with atherogenic-modified lipoproteins, fa- voring the formation of foam cells, and exerting a proin- flammatory action. Pentraxin serum levels have been shown to be associated with clinical and subclinical atherosclerosis in general population. Antibodies against pentraxins have been demonstrated in patients with autoimmune diseases, but their role in atherogenesis is still controversial. Keywords Atherosclerosis . Pentraxins . Autoimmunity . Autoantibodies . Complement system . Anti-pentraxins autoantibodies Atherosclerosis is a complex pathological process of the vascular wall, which predominantly affects large and medium-sized arteries, leading to peripheral vascular disease, angina pectoris, cardiovascular failure, myocardial infarction, transitory ischemic attack, and stroke. It repre- sents the main cause of death in western and industrialized countries. For many years, atherosclerosis was considered a degenerative disease caused by a bland lipid storage in the vessels; but in the last decades, several groups have demonstrated that it is a process closely related to inflammation, involving mechanisms of both innate and adaptive immunity [1–4]. Epidemiological and cohort studies demonstrated that not only traditional risk factors for atherosclerosis but also chronic infections, inflammatory, and immune factors, including cytokines, chemokines, T and B cells, and even autoantibodies are involved in atherogenesis [1–5]. Interestingly, atherosclerosis is accelerated in many autoimmune conditions such as systemic lupus erythemato- sus and rheumatoid arthritis [6–8]. Many autoantibodies and their cognate antigens may be involved in atherogenesis [9– 11], including pentraxins and autoantibodies against pen- traxins [12, 13]. The aim of this paper is to give an overview of the potential role of pentraxins and anti-pentraxins autoanti- bodies in the induction and progression of atherosclerosis. Immune-inflammatory mechanisms involved in atherogenesis There is clear evidence that both innate and adaptive immunity play a role in atherogenesis [2–10]. The first step of this process is the activation of endothelial cells leading to a proinflammatory phenotype characterized by an Clinic Rev Allerg Immunol (2009) 37:36–43 DOI 10.1007/s12016-008-8098-6 N. Bassi : S. Zampieri : A. Ghirardello : M. Tonon : M. Zen : F. Cozzi : A. Doria (*) Division of Rheumatology, Department of Medical and Surgical Sciences, University of Padova, Via Giustiniani, 2, 35128 Padova, Italy e-mail: adoria@unipd.it