Determinants of vessel targeting in vasculitis.
Studies of autoimmune diseases have not yet elucidated why certain organs or vessels become the objects of injury while others are spared. This paper explores the hypothesis that important differences exist in regions of the aorta; these regional variations determine vulnerability to such diseases as atherosclerosis, aortitis, giant-cell arteritis, and Takayasu's disease. The reader is invited to reassess two issues: (1) whether the aorta is indeed a single homogeneous structure; and (2) whether the initial stage of aortitis (and indeed other diseases considered "autoimmune") may primarily be the result of acquired alterations of substrate that influence unique immune profiles, but that by themselves may not be pathogenic. Disease susceptibility and patterns are influenced by many factors that are either inborn or acquired. Examples include genetic background, gender, ethnicity, aging, prior and concomitant illnesses, habits, diet, and exposure to toxins and other environmental hazards. Studies of vascular diseases must assess how such variables affect regional anatomic differences in endothelial cells, subendothelial matrix, and vascular smooth muscle, as well as the response of each to a variety of stimuli.
Hoffman
Gary S
GS
Department of Rheumatic and Immunologic Diseases, Center for Vasculitis Care and Research, Cleveland Clinic Foundation A50, Cleveland, OH 44195, USA. hoffmag@ccf.org
D000375:Aging / Q000276:immunology; D000818:Animals; D001025:Aortitis / Q000209:etiology; D050197:Atherosclerosis / Q000209:etiology; D003094:Collagen / Q000502:physiology; D004195:Disease Models, Animal; D004549:Elastin / Q000502:physiology; D013700:Giant Cell Arteritis / Q000209:etiology; D006801:Humans; D007107:Immune System / Q000502:physiology; D013625:Takayasu Arteritis / Q000209:etiology; D014657:Vasculitis / Q000209:etiology*
D003094:Collagen; D004549:Elastin