Adult-onset Still's disease pathophysiology
Template:Adult-onset Still's disease
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Pathophysiology
Adult-onset Still's disease is an automminue inflammatory arthritis that typically affects adolescents and adults ranging from age 16-40 years. Major etiological mechanisms behind cause a dysfunction of the innate and cellular immunity (limited) leading to activation of effector cells of the disease.
Putative triggers
Immune dysfunction
Role of interleukin-1 beta
Interleukin-i beta plays a key role in producing major characteristic features of adult-onset Still's disease. The following processes are affected by an increased production of this key interleukin:
Hypothalamic-pituitary axis influence
Liver synthesis and secretion of acute phase proteins
Osteoclasts activation and matrix metalloproteinases (MMPs) synthesis
Innate immune system cells activation
Increased gene transcription of proinflammatory molecules