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1 some-related genes might be involved in this autoinflammatory syndrome.
2 n healthy control subjects and patients with autoinflammatory syndrome.
3 editerranean fever, 2 archetypical monogenic autoinflammatory syndromes.
4 Point mutations in NLRC4 cause autoinflammatory syndromes.
5 lease is central to the pathogenesis of many autoinflammatory syndromes.
6 une system activation owing to infections or autoinflammatory syndromes.
7 le dermatomyositis, juvenile scleroderma and autoinflammatory syndromes.
8 ovide insights regarding the pathogenesis of autoinflammatory syndromes.
9 from gene mutations is related to monogenic autoinflammatory syndromes.
10 the adaptive immune system in patients with autoinflammatory syndromes.
11 in NLRP3 are associated with recurrent fever/autoinflammatory syndromes.
13 patients have mutations in the cold-induced autoinflammatory syndrome 1 (CIAS1) gene, encoding cryop
14 me, also known as "cryopyrin," "cold-induced autoinflammatory syndrome 1" (CIAS1), or nacht domain-,
15 such as Muckle-Wells syndrome, familial cold autoinflammatory syndrome and urate crystal-induced peri
16 ious potential complication of the inherited autoinflammatory syndromes and frequently results in end
18 d inflammasome activation is associated with autoinflammatory syndromes and several common diseases.
20 orders: Muckle-Wells syndrome, familial cold autoinflammatory syndrome, and chronic infantile neurolo
22 s on recent progress in our understanding of autoinflammatory syndromes, and how insights into these
23 ations in inflammasome-related genes lead to autoinflammatory syndromes, and review the contribution
25 r-associated periodic syndrome (TRAPS) is an autoinflammatory syndrome associated with mutations in t
26 onocytes expressing familial cold-associated autoinflammatory syndrome-associated Cryopyrin mutations
27 and IL1RN, cause two severe and early-onset autoinflammatory syndromes, CAPS (cryopyrin associated p
29 tugal and Mexico with an autosomal-recessive autoinflammatory syndrome characterized by joint contrac
30 4416) is a rare autosomal dominant inherited autoinflammatory syndrome characterized by pyogenic ster
34 yndrome (MWS), 18 with familial cold-induced autoinflammatory syndrome (FCAS), and 3 probands with MW
35 s Muckle-Wells syndrome (MWS), familial cold autoinflammatory syndrome (FCAS), and neonatal-onset mul
36 flammatory disorders including familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome
38 New models for the pathogenesis of several autoinflammatory syndromes have been proposed, including
39 and clinical characterizations of monogenic autoinflammatory syndromes have led to ground breaking i
40 d acne; Muckle-Wells syndrome; familial cold autoinflammatory syndrome; immunodysregulation, polyendo
41 ic juvenile idiopathic arthritis (JIA) is an autoinflammatory syndrome in which the myelomonocytic li
42 mation and thus novel therapeutic targets in autoinflammatory syndromes including other IL-1beta medi
43 IRA have encouraged their wider use in other autoinflammatory syndromes including the classic heredit
44 ee autoinflammatory disorders: familial cold autoinflammatory syndrome, Muckle-Wells syndrome and neo
45 cryopyrin are associated with familial cold autoinflammatory syndrome, Muckle-Wells syndrome and neo
49 elevated temperature (CANDLE syndrome) is an autoinflammatory syndrome recently described in children
50 g genetic and clinical spectrum of TRAPS, an autoinflammatory syndrome resulting from mutations in th
51 ans, NLR mutations are often associated with autoinflammatory syndromes, suggesting a complex role fo
52 c syndrome (TRAPS) is a dominantly inherited autoinflammatory syndrome that results from mutations in
53 cal and pathogenic description of this novel autoinflammatory syndrome, thereby expanding the clinica
54 ctrum of diseases ranging from familial cold autoinflammatory syndrome to Muckle-Wells syndrome to NO
55 uses Muckle-Wells syndrome and familial cold autoinflammatory syndrome, two dominantly inherited diso
56 cial role of IL-1beta in the pathogenesis of autoinflammatory syndromes, we hypothesized that IL-1bet
57 witched B cells and 'IgD-armed' basophils in autoinflammatory syndromes with periodic fever, our data
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