Psoriasis is an inflammatory skin disease whose pathophysiology is attributed to both innate and adaptive immune cells and molecules. Despite the crucial roles of the immune system in psoriasis, it cannot be categorized as an autoimmune disease because of the lack of main signs of autoimmunity, such as specific antibodies, well-defined antigens, and autoimmune genetic risk factors. The presence of some cellular and molecular properties, such as the presence of neutrophils in skin lesions and the activation of the innate immune system, attributes psoriasis to a group of diseases called autoinflammatory disorders. Autoinflammatory diseases refer to a group of inherited disorders whose main manifestations are recurrent fever, a high level of acute-phase reactant, and a tendency for inflammation of the skin, joints, and other organs like the nervous system. In most autoinflammatory disorders, it has been seen that complexes of the high-molecular-weight protein named inflammasomes have significant roles. The inflammasome complex usually is formed and activated in the stimulated immune cell cytoplasm, and its activation consequently leads to inflammatory events such as producing of active caspase-1, mature interleukin-1β (IL-1β), and IL-18 and can cause an inflammatory programmed cell death called pyroptosis. Since the identification of inflammasomes, it has been shown that there are close links between them and hereditary and acquired autoinflammatory diseases like psoriasis. In this review, we aim to focus on well-defined inflammasome and their role in the pathophysiology of psoriasis.
Keywords: Cell death; Inflammasomes; Interleukin-1β; NLRP3; Psoriasis; Pyroptosis.
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