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Ravet, N., Rouaghe, S., Dode, C., Bienvenu, J., Stirnemann, J., Levy, P., Delpech, M. and Grateau, G. (2006) Clinical significance of P46L and R92Q substitutions in the tumour necrosis factor superfamily 1A gene. Annals of the Rheumatic Diseases, 65, 1158-1162. http://dx.doi.org/10.1136/ard. 2005.048611

has been cited by the following article:

• TITLE: Autoinflammatory diseases in childhood

  AUTHORS: Betul Sozeri, Ozgur Kasapcopur

  KEYWORDS: Autoinflammatory Diseases; Familial Mediterranean Fever; Diagnosis; Pathogenesis; Treatment

  JOURNAL NAME: Modern Research in Inflammation, Vol.3 No.1, February 11, 2014

  ABSTRACT: Autoinflammatory diseases are defined as recurrent attacks of systemic inflammation that are often unprovoked (or triggered by a minor event) related to a lack of adequate regulation of the innate immune system. Within the past decade, the list of autoinflammatory diseases has included cryopyrin-associated periodic syndromes, familial Mediterranean fever, mevalonate kinase deficiency, tumor necrosis factor receptor-associated periodic syndrome, hereditary pyogenic disorders, pediatric granulomatous autoinflammatory diseases, idiopathic febrile syndromes (systemic-onset juvenile idiopathic arthritis, PFAPA syndrome), complement dysregulation syndromes and Behcet’s disease. The hereditary autoinflammatory diseases are a group of Mendelian disorders characterized by seemingly unprovoked fever and localized inflammation. Autoinflammatory diseases can activate NOD-like receptors and inflammasome products including especially interleukin 1β. In this review, it focuses on how recent advances have impacted hereditary autoinflammatory diseases.