TY - JOUR
T1 - Untangling the web of systemic autoinflammatory diseases
AU - Rigante, Donato
AU - Lopalco, Giuseppe
AU - Vitale, Antonio
AU - Lucherini, Orso Maria
AU - Caso, Francesco
AU - De Clemente, Caterina
AU - Molinaro, Francesco
AU - Messina, Mario
AU - Costa, Luisa
AU - Atteno, Mariangela
AU - Laghi-Pasini, Franco
AU - Lapadula, Giovanni
AU - Galeazzi, Mauro
AU - Iannone, Florenzo
AU - Cantarini, Luca
PY - 2014
Y1 - 2014
N2 - The innate immune system is involved in the pathophysiology of systemic autoinflammatory diseases (SAIDs), an enlarging group of disorders caused by dysregulated production of proinflammatory cytokines, such as interleukin-1β and tumor necrosis factor-α, in which autoreactive T-lymphocytes and autoantibodies are indeed absent. A widely deranged innate immunity leads to overactivity of proinflammatory cytokines and subsequent multisite inflammatory symptoms depicting various conditions, such as hereditary periodic fevers, granulomatous disorders, and pyogenic diseases, collectively described in this review. Further research should enhance our understanding of the genetics behind SAIDs, unearth triggers of inflammatory attacks, and result in improvement for their diagnosis and treatment.
AB - The innate immune system is involved in the pathophysiology of systemic autoinflammatory diseases (SAIDs), an enlarging group of disorders caused by dysregulated production of proinflammatory cytokines, such as interleukin-1β and tumor necrosis factor-α, in which autoreactive T-lymphocytes and autoantibodies are indeed absent. A widely deranged innate immunity leads to overactivity of proinflammatory cytokines and subsequent multisite inflammatory symptoms depicting various conditions, such as hereditary periodic fevers, granulomatous disorders, and pyogenic diseases, collectively described in this review. Further research should enhance our understanding of the genetics behind SAIDs, unearth triggers of inflammatory attacks, and result in improvement for their diagnosis and treatment.
KW - Autoinflammation
KW - Interleukin-1
KW - Autoinflammation
KW - Interleukin-1
UR - http://hdl.handle.net/10807/62926
U2 - 10.1155/2014/948154
DO - 10.1155/2014/948154
M3 - Article
SN - 1466-1861
VL - 2014
SP - N/A-N/A
JO - Mediators of Inflammation
JF - Mediators of Inflammation
ER -