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1 TRAPS is caused by dominantly inherited mutations in TNF
2 TRAPS is caused by missense mutations in the extracellul
3 TRAPS mutant TNFR1 molecules were retained intracellular
4 TRAPS-associated mutant and wild-type TNFRSF1A behaved d
5 TRAPS-associated mutant TNFRSF1A has an antigenically al
6 TRAPS-associated TNFRI mutants induce the expression of
7 l fibroblasts, but not leukocytes, from C33Y TRAPS patients demonstrated reduced shedding of TNFRSF1A
8 d dermal fibroblasts from patients with C33Y TRAPS, and in HEK 293 cell lines stably transfected with
11 a suggest a new hypothesis, in that the C43S TRAPS mutation may cause the inflammatory phenotype by i
14 was completely abolished by the C33Y or C52F TRAPS-associated mutations, whereas other mutations (T50
15 e and clinical differences between different TRAPS-associated mutants of TNFRSF1A result from differe
16 functional alterations caused by 9 distinct TRAPS-associated TNFR1 mutations in transfected cells an
19 and peripheral blood mononuclear cells from TRAPS patients relative to those from healthy controls.
20 t WT and mutant forms of TNFRI, derived from TRAPS patients, interact in the absence of TNF ligand.
25 L-6 in mediating the inflammatory attacks in TRAPS, but blockade of IL-6 did not affect the underlyin
27 Evidence for nonallelic heterogeneity in TRAPS-like conditions was found: 3 members of the "proto
32 t some of the inflammatory processes seen in TRAPS do not involve direct interaction of TNF with its
34 ese findings demonstrate the need to include TRAPS in the differential diagnosis of recurrent fevers
36 The patient, a 52-year-old man with lifelong TRAPS in whom treatment with etanercept and anakinra had
40 rly in peripheral blood mononuclear cells of TRAPS patients and in multiple cell types from two indep
43 and serum levels of inflammatory markers of TRAPS in a dose-dependent manner, but does not completel
45 ntracellular retention in the neutrophils of TRAPS patients with the C33Y mutation, with little if an
48 loidosis and indicated a lower penetrance of TRAPS symptoms in individuals with noncysteine mutations
51 broadening genetic and clinical spectrum of TRAPS, an autoinflammatory syndrome resulting from mutat
55 of inflammatory diseases, such as FMF, PAPA, TRAPS, and HIDS, has elucidated the pathophysiology of t
58 actor receptor-associated periodic syndrome (TRAPS) is a dominantly inherited autoinflammatory syndro
59 actor receptor-associated periodic syndrome (TRAPS) is an autoinflammatory syndrome associated with m
60 (TNF) receptor-associated periodic syndrome (TRAPS) is an autosomal dominant systemic autoinflammator
61 eceptor (TNFR)-associated periodic syndrome (TRAPS) is an autosomal-dominant autoinflammatory conditi
62 actor receptor-associated periodic syndrome (TRAPS) is an autosomal-dominant autoinflammatory conditi
63 actor receptor-associated periodic syndrome (TRAPS) is an inherited autosomal-dominant autoinflammato
64 RSF1A) in TNFR-associated periodic syndrome (TRAPS) on the binding of anti-TNFRSF1A monoclonal antibo
65 actor receptor-associated periodic syndrome (TRAPS) treated with the anti-interleukin-6 (anti-IL-6) r
66 actor receptor-associated periodic syndrome (TRAPS), an autoinflammatory disorder caused by missense
67 , TNF-receptor-associated periodic syndrome (TRAPS), presents with prolonged attacks of fever and sev
68 actor receptor-associated periodic syndrome (TRAPS), whilst both spontaneous and pathogen-associated
71 actor receptor-associated periodic syndrome (TRAPS); informative markers spanning the TNFRSF1A locus
73 lammation, define a periodic-fever syndrome, TRAPS (TNF receptor-associated periodic syndrome [MIM 14
78 ultiple members had symptoms compatible with TRAPS and in 176 consecutive subjects with sporadic (non
79 the myalgia experienced by individuals with TRAPS is due to a monocytic fasciitis and not to myositi
80 be herein the case of a 60-year-old man with TRAPS, in whom magnetic resonance imaging of the left th
81 l TNFRSF1A mutation (C43S) in a patient with TRAPS and to examine the effects of this TNFRSF1A mutati
82 f cysteine mutations, 13 of 14 patients with TRAPS and amyloidosis and indicated a lower penetrance o
83 Peripheral blood obtained from patients with TRAPS and healthy control subjects was stained with mono
84 s in the clinical phenotype of patients with TRAPS may be attributable to variable effects of TNFRSF1
85 6 expression by monocytes from patients with TRAPS was not attributable to a defect in activation-ind
87 n by monocytes was elevated in patients with TRAPS, as a feature of the underlying constitutive infla
88 was significantly elevated in patients with TRAPS, even though the patients were not experiencing cl
89 retention in the leukocytes of patients with TRAPS, which is consistent with previous findings from i
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