Free Hemoglobin: a Dangerous Signal for the Immune System in Patients with Carotid Atherosclerosis?
From: Dipartimento di Malattie Infettive, Parassitarie ed Immunomediate, Istituto Superiore di Sanità , Rome, Italy. rachele.rigano@iss.it.
Annals of the New York Academy of Sciences
- Publish Date: Jun 2007
- ISSN: 0077-8923
- Volume: 1107
- Issue:
- Pages: 42-50
- Medium: Print
- Language: English
- Citation (JAMA): Buttari Brigitta, Profumo Elisabetta, Petrone Linda, et al. Free Hemoglobin: a Dangerous Signal for the Immune System in Patients with Carotid Atherosclerosis?. Ann. N. Y. Acad. Sci. Jun 2007;1107:42-50
Abstract
Atherosclerosis is a chronic inflammatory multifactorial disease in which immune responses are key pathogenetic factors. T cell-mediated immunity contributes to the initiation and progression of atherosclerotic disease, but the nature of antigens responsible for immune cell activation is still not completely elucidated. Convincing evidence supports a determinant role of autoimmune responses to self-structures in shaping the progression of the disease. Autoimmune responses may be directed against altered self-structures, such as oxidized low-density lipoproteins (LDL). Oxidative stress, increasingly reported in patients with atherosclerosis, is the major event causing protein structural modification, thus inducing the appearance of neo/cryptic epitopes on the molecule. Intraplaque hemorrhage, a common event in advanced lesions, causes the deposition of large amounts of hemoglobin (Hb). The pro-oxidative intraplaque microenvironment may induce structural changes in extra-erythrocytic free Hb, thus generating novel/cryptic autoantigenic epitopes. We demonstrated that an oxidized Hb preparation enriched in hemichromes expands IFN-gamma-secreting T lymphocytes in patients with advanced carotid atherosclerosis and enhances the phenotypical and functional maturation of human monocyte-derived dendritic cells induced by lipopolysaccharide (LPS). Overall, our findings suggest that oxidized forms of Hb could act as a dangerous signal for the immune system, thus contributing to the inflammatory process that takes place within the atherosclerotic plaque.
Mesh Headings (Keywords): Adaptation, Biological, Animals, Atherosclerosis, Autoantigens, Carotid Artery Diseases, Hemoglobins, Humans, Immune System, Immunity, Natural
Check for Full Text / PubMed Unique Identifier (PMID): 17804531
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