[Giant-cell arteritis pathogenesis]. 2012

Maxime Samson, and Bernard Bonnotte
CHU de Dijon, service de médecine interne et immunologie clinique, 21000 Dijon, France.

Giant-cell arteritis (GCA) involves larges arteries, especially aorta and extra-cranial branches of external carotid. Histo-pathological lesions affect all the layers of the artery leading to a segmental and focal panarteritis with a polymorphic cell infiltrate including T cells, macrophages and multinucleated giant cells, a fragmented internal elastic lamina and an intimal hyperplasia. The pathophysiology of GCA is not fully understood. After dendritic cell activation in the adventitia, CD4T cells are recruited in the arterial wall and polarized into Th1 and Th17 cells that produce IFN-γ and IL-17. These cytokines activate macrophages, giant cells and smooth muscle cells inducing vascular remodeling leading to ischemic manifestations of GCA. Macrophages infiltrating the adventitia produce IL-1β and IL-6 that are responsible for general symptoms encountered in GCA. In this review, we discuss GCA pathogenesis, with emphasis on the role of IL-6 as a promising therapeutic target.

UI MeSH Term Description Entries
D008954 Models, Biological Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment. Biological Model,Biological Models,Model, Biological,Models, Biologic,Biologic Model,Biologic Models,Model, Biologic
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000375 Aging The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time. Senescence,Aging, Biological,Biological Aging
D013700 Giant Cell Arteritis A systemic autoimmune disorder that typically affects medium and large ARTERIES, usually leading to occlusive granulomatous vasculitis with transmural infiltrate containing multinucleated GIANT CELLS. The TEMPORAL ARTERY is commonly involved. This disorder appears primarily in people over the age of 50. Symptoms include FEVER; FATIGUE; HEADACHE; visual impairment; pain in the jaw and tongue; and aggravation of pain by cold temperatures. (From Adams et al., Principles of Neurology, 6th ed) Aortic Arteritis, Giant Cell,Aortitis, Giant Cell,Arteritis, Temporal,Cranial Arteritis,Horton Disease,Horton Giant Cell Arteritis,Juvenile Temporal Arteritis,Temporal Arteritis,Arteritis, Giant Cell, Horton,Arteritis, Giant Cell, Horton's,Giant Cell Aortic Arteritis,Giant Cell Aortitis,Giant Cell Aortitis, Horton's,Giant Cell Arteritis, Horton,Horton's Disease,Horton's Giant Cell Arteritis,Aortitides, Giant Cell,Arteritides, Cranial,Arteritides, Giant Cell,Arteritides, Juvenile Temporal,Arteritides, Temporal,Arteritis, Cranial,Arteritis, Giant Cell,Arteritis, Juvenile Temporal,Cranial Arteritides,Giant Cell Aortitides,Giant Cell Arteritides,Hortons Disease,Juvenile Temporal Arteritides,Temporal Arteritides,Temporal Arteritides, Juvenile,Temporal Arteritis, Juvenile
D015850 Interleukin-6 A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS. Hepatocyte-Stimulating Factor,Hybridoma Growth Factor,IL-6,MGI-2,Myeloid Differentiation-Inducing Protein,Plasmacytoma Growth Factor,B Cell Stimulatory Factor-2,B-Cell Differentiation Factor,B-Cell Differentiation Factor-2,B-Cell Stimulatory Factor 2,B-Cell Stimulatory Factor-2,BSF-2,Differentiation Factor, B-Cell,Differentiation Factor-2, B-Cell,IFN-beta 2,IL6,Interferon beta-2,B Cell Differentiation Factor,B Cell Differentiation Factor 2,B Cell Stimulatory Factor 2,Differentiation Factor 2, B Cell,Differentiation Factor, B Cell,Differentiation-Inducing Protein, Myeloid,Growth Factor, Hybridoma,Growth Factor, Plasmacytoma,Hepatocyte Stimulating Factor,Interferon beta 2,Interleukin 6,Myeloid Differentiation Inducing Protein,beta-2, Interferon
D056724 Immunity, Humoral Antibody-mediated immune response. Humoral immunity is brought about by ANTIBODY FORMATION, resulting from TH2 CELLS activating B-LYMPHOCYTES, followed by COMPLEMENT ACTIVATION. Humoral Immune Response,Humoral Immune Responses,Humoral Immunity,Immune Response, Humoral,Immune Responses, Humoral,Response, Humoral Immune
D058990 Molecular Targeted Therapy Treatments with drugs which interact with or block synthesis of specific cellular components characteristic of the individual's disease in order to stop or interrupt the specific biochemical dysfunction involved in progression of the disease. Targeted Molecular Therapy,Molecular Targeted Therapies,Molecular Therapy, Targeted,Targeted Molecular Therapies,Targeted Therapy, Molecular,Therapy, Molecular Targeted,Therapy, Targeted Molecular

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