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Wise, C.A., Gillum, J.D., Seidman, C.E., Lindor, N.M., Veile, R., Bashiardes, S. and Lovett, M. (2002) Mutations in CD2BP1 disrupt binding to PTP PEST and are responsible for PAPA syndrome, an autoinflammatory disorder. Human Molecular Genetics, 11, 961-969. http://dx.doi.org/10.1093/ hmg/11.8.961

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.