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1 tivity indicates that TNFR:Fc functions as a TNF antagonist.
2 autoimmune" disease effectively treated with TNF antagonists.
3 oped new-onset heart failure after receiving TNF antagonists.
4 ministration-approved tumor necrosis factor (TNF) antagonists.
5  soluble TNFRIIFc (a dimorphic high-affinity TNF antagonist); (4) mice expressing TNFRIIFc transgene
6 evaluated the safety and efficacy of a novel TNF antagonist - a recombinant fusion protein that consi
7 rly combined immunosuppression (ECI), with a TNF antagonist and antimetabolite might be a more effect
8 fluorocitrate (a glial metabolic inhibitor), TNF antagonist, and IL-1 antagonist each blocked gp120-i
9  p75 has been proposed to function as both a TNF antagonist by neutralizing TNF and as a TNF agonist
10 ith systemic juvenile arthritis treated with TNF antagonists display overexpression of IFN-alpha-regu
11                                     IL-1 and TNF antagonists each prevented gp120-induced pain change
12 potential efficacy of etanercept, a specific TNF antagonist (Enbrel).
13   Treatment starting 2 d before SNL with the TNF antagonist etanercept (1 mg, i.p., every third day)
14                Preemptive treatment with the TNF antagonist etanercept reduced SNL-induced allodynia
15 analysis involved 315 patients with previous TNF antagonist failure (ie, an inadequate response to, l
16  higher proportion of patients with previous TNF antagonist failure given vedolizumab also had a CDAI
17  Among patients who had experienced previous TNF antagonist failure, 15.2% of those given vedolizumab
18                   Systemic administration of TNF antagonists for radiculopathy in the clinic has show
19 ted the safety and efficacy of etanercept, a TNF antagonist, for the treatment of plaque psoriasis.
20 severe Crohn's disease that was resistant to TNF antagonists had an increased rate of response to ind
21 ents with CD in whom previous treatment with TNF antagonists had failed.
22 previous therapy with tumor necrosis factor (TNF) antagonists has failed.
23 disease and consideration of a change in the TNF antagonist if the lesions are unresponsive to conven
24 s represent potential therapeutic targets of TNF antagonists in psoriasis.
25 patients treated with tumor necrosis factor (TNF) antagonists indicate that this is not a rare phenom
26                                              TNF antagonist-induced psoriasis is a newly recognized a
27                       Three infusions of the TNF antagonist infliximab (5 mg/kg) (n = 30) or placebo
28  Crohn disease who are naive to the chimeric TNF antagonist, infliximab.
29 imumab, a fully human tumor necrosis factor (TNF) antagonist, is an effective treatment for patients
30 gs (DMARDs), such as tumour necrosis factor (TNF) antagonists, is associated with a reduced risk of C
31                   In a fraction of patients, TNF antagonists might induce new-onset heart failure or
32 ondary nonresponse to tumor necrosis factor (TNF) antagonists or had unacceptable side effects.
33 OUND & AIMS: Although tumor necrosis factor (TNF) antagonists reduce many clinical features of inflam
34 umor necrosis factor (TNF)-alpha receptor, a TNF antagonist; septic patients were also studied.
35 een shown, and consequently various types of TNF antagonists such as etanercept and infliximab have b
36 pt and infliximab are tumor necrosis factor (TNF) antagonists that have been recently approved for th
37                  Because sTNFRIIs can act as TNF antagonists, the association between recipient and d
38 e role of alternative tumor necrosis factor (TNF) antagonist therapies in the context of failure of i
39  (N = 416), which included patients naive to TNF antagonist therapy (n = 101).
40 erapies in the context of failure of initial TNF antagonist therapy in patients with rheumatoid arthr
41 the pathogenesis of rheumatoid arthritis and TNF antagonist therapy represent successes of immunology
42                                        After TNF antagonist therapy was discontinued and heart failur
43                                        After TNF antagonist therapy, 38 patients developed new-onset
44 iasis may occur any time after initiation of TNF antagonist therapy, is often of an uncommon morpholo
45 ere evaluated before and after initiation of TNF antagonist therapy.
46 I IFN activity might predict the response to TNF antagonist therapy.
47 re predictive of the therapeutic response in TNF antagonist-treated RA patients, indicating that thes
48  loss of response to, or intolerance of >/=1 TNF antagonists); we determined the proportion of patien
49  the same center who were not treated with a TNF antagonist were studied.
50 (HF) would be beneficial, clinical trials of TNF antagonists were paradoxically negative.
51 ed with at least one tumour necrosis factor (TNF) antagonist (which had failed in 96 [79%]).
52 duct, and stratified by previous exposure to TNF antagonists (yes vs no).

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