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1 TNF activates opposing pathways leading to caspase-8-med
2 TNF has been reported to increase entry of HCV pseudopar
3 TNF inhibited completion of the HCV infectious cycle in
4 TNF plays an integral role in inflammatory bowel disease
5 TNF receptor-associated death domain (TRADD) is an essen
6 TNF receptor-associated factor 6 (TRAF6) is identified a
7 TNF was also required during the allergen challenge phas
8 TNF-alpha (but not IL5, IL-3, eotaxin-1 or GM-CSF) was d
9 TNF-alpha is a pluripotent cytokine that has been indepe
10 TNF-alpha related apoptosis-inducing ligand (TRAIL) sele
11 TNF-alpha treatment of colonic rho(0) cells augmented IL
12 TNF-alpha was not detected in Muller cells from diabetic
13 TNF-related apoptosis-inducing ligand (TRAIL) is a death
14 TNF-related apoptosis-inducing ligand (TRAIL) was initia
15 TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) has
16 monocyte chemoattractant protein 1 (MCP-1), TNF-alpha, and IL-6 and hepatic cleaved caspase 3 in mic
17 s tested but urokinase was released by IL-1, TNF-alpha, and thrombin (positive control), but not estr
19 6, FOXP3), cytokines (IL-1beta, IL-6, IL-10, TNF-alpha) and oxidative stress (superoxide dismutase, c
23 jun and p38 activation, as well as IL-1beta, TNF-alpha, and IL-10 secretion in vascular endothelial c
24 induced a significant increase in IL-1beta, TNF-alpha, and IL-6 messenger RNA (mRNA) expression and
27 ted with reduced inflammation (MCP-1, MIP-2, TNF-alpha, IL-6 and CD68), decreased accumulation of bon
28 IKK-beta, TNF receptor-associated factor 6, TNF receptor-associated factor 2, receptor-interacting p
29 orn to obese mothers generate a reduced IL-6/TNF-alpha response to TLR 1/2 and 4 ligands compared to
31 a higher false alarm metric in this abnormal TNF signaling system indicates perceiving more cytokine
33 ide (AICAR), on tumor necrosis factor alpha (TNF-alpha) induction of complement factor B (CFB) in RPE
34 he detection of tumor necrosis factor alpha (TNF-alpha) within the randomly chosen range of 266pg/mL
36 on (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin 2 (IL-2) secretion by CD8(+)
37 kin (IL) 1beta, tumor necrosis factor alpha (TNF-alpha), CXCL10, CCL5, IL-6, and superoxide dismutase
38 treatment with tumor necrosis factor alpha (TNF-alpha)-neutralizing antibodies decreased the frequen
39 e production of tumor necrosis factor alpha (TNF-alpha)/interleukin-6 (IL-6) in infected kidneys.
40 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha) play key roles in progression of renal fibros
41 wnregulation of tumor necrosis factor-alpha (TNF-alpha) production and concomitant upregulation of NF
43 ression of A20 (tumor necrosis factor alpha [TNF-alpha]-induced protein 3 [TNFAIP3]), an inhibitor of
45 markers synergistically induced by IL-17 and TNF-alpha (IL-17A/C, IL-19, CXCL1, PI3, CCL20, and IL36G
49 ar translocation and downstream IL-1beta and TNF-alpha protein production following TLR2 receptor sti
50 ctional analysis revealed defective IL-2 and TNF production yet retained expression of IFN-gamma and
52 ibrinogen, the expression levels of IL-6 and TNF-alpha in integrin alphaM(PS)beta2 BMDMs were signifi
56 uctions of IL-17 and IL-23, but not IL-6 and TNF-alpha, whereas IL-10 levels were increased in periph
58 appaB (nuclear factor-kappaB) activation and TNF (tumor necrosis factor) production by myeloid cells.
59 However, T. gondii inhibited IFN-alpha and TNF-alpha produced in response to HSV and HIV, thus func
60 vity also failed to up-regulate IFN-beta and TNF-alpha after treatment with DMXAA or the natural STIN
62 ect of EtOH on IL-15, RANTES, TGF-beta1, and TNF-alpha cytokines while restoring MCP-2 levels, sugges
64 iated with increased cytotoxic character and TNF and IFNgamma production upon target-cell recognition
65 thways activated in human inflamed colon and TNF-alpha-treated cells (false discovery rate < 0.05).
66 n murine enteroids and colonoid cultures and TNF-induced beta-catenin activation in nontransformed hu
70 vo atherosclerotic tissue with IFN-gamma and TNF-alpha and found they synergistically increased monoc
71 early correlated inhibition of IFN-gamma and TNF-alpha production, along IL-10 increase, (ii) CD73(+)
72 that naive CAST mice make low IFN-gamma and TNF-alpha responses and have low levels of NK cells and
73 the pro-inflammatory cytokines IFN-gamma and TNF-alpha synergistically up-regulated PD-L1 expression.
74 on decreased the production of IFN-gamma and TNF-alpha, T cell proliferation, and the expression of C
77 re collected and analyzed histologically and TNF protein levels measured by enzyme-linked immunosorbe
78 signaling crosstalk between interferons and TNF is integrated at the level of chromatin to reprogram
81 nt particle sizes with dyes/QDs for LCN1 and TNF-alpha, we successfully used REP to detect the two DR
82 ation of p65, and suppressed basal level and TNF-alpha-induced expression of chemokines and adhesion
83 tream of NF-kappaB-inducing kinase (NIK) and TNF receptor family members including lymphotoxin-beta r
85 T signalling system (5-HT, 5-HIAA, SERT) and TNF-alpha expression were examined in the distal colon o
88 ble to mount an immune response against anti-TNF-alpha Abs, suggesting that immune complexes are a ma
90 nt with both immunosuppressant (IS) and anti-TNF before colectomy was independently associated with I
91 alent binding of capturing biomolecule (anti-TNF-alpha antibody) on off-surface matrix was achieved v
93 ncrease in postoperative complications, anti-TNF agent use within 90 days of surgery among patients w
94 ement in endothelial function following anti-TNF-alpha treatment (SDM 0.987, 95%CI [0.64-1.33], p < 0
96 y; in FcgammaR(-/-)Rag1(-/-) mice given anti-TNF these numbers were as low as FcgammaR(-/-)Rag1(-/-)
97 To determine the efficacy and safety of anti-TNF in treating cutaneous sarcoidosis in a large observa
101 , 2.35; 95% CI, 1.31-4.22; P < .001) or anti-TNF monotherapy (aHR, 2.53; 95% CI, 1.35-4.77; P < .001)
102 D, the use of thiopurine monotherapy or anti-TNF monotherapy was associated with a small but statisti
104 olons from Rag1(-/-) mice that received anti-TNF had an increased number of CD206(+) macrophages comp
107 tudies, our meta-analysis suggests that anti-TNF-alpha treatment may improve endothelial function in
109 is who were refractory or intolerant to anti-TNF drugs and other biological treatments, both dosing r
110 , 0.41-0.67), 32 in patients exposed to anti-TNF monotherapy (IR, 0.41; 95% CI, 0.27-0.55), and 14 in
111 ortunately, not all patients respond to anti-TNF therapy, and some patients show paradoxical immune s
115 ns in the treatment of RA patients with anti-TNF-alpha drugs and in the potential use of TNF-targeted
116 ncluding RA patients; 3) treatment with anti-TNF-alpha medications; 4) evaluating the change from bas
117 thelial integrity, while treatment with anti-TNF-alpha or anti-IL-4Ralpha monoclonal antibodies resto
118 provide evidence that MenA inhibitors act as TNF-alpha and IL-6 inhibitors, raising the potential for
122 tegrity, while knockdown of USP48 attenuates TNF-alpha/JNK pathway and increases E-cadherin expressio
123 otein interactions with IKK-alpha, IKK-beta, TNF receptor-associated factor 6, TNF receptor-associate
127 onally to its local actions in the AD brain, TNF-alpha can also indirectly modulate amyloid pathology
131 icated activation of pulmonary macrophage by TNF-alpha and/or MCP-1 in the mechanisms of RSV-induced
132 reases, such as: MMP9 correlated with CCL22, TNF, FASL, RUNX3, and SEMAD4 in AdMSC and, in T cells, M
133 dings establish a mechanism by which chronic TNF-alpha signaling orchestrates a functional interplay
134 e formation of the TNF-R1 signaling complex (TNF-RSC) to mediate downstream cellular fate decision.
136 ed upregulation of pro-inflammatory cytokine TNF-alpha in an ImI concentration-dependent manner from
137 able to dose dependently stimulate cytokine TNF-alpha, IL-1beta, IL-6, IL-10, and IL-12 production i
138 es showed that the proinflammatory cytokines TNF and type I interferons induced transcriptional casca
142 n of TNF receptor (TNFR)-1 and -2, decreased TNF-alpha-induced phosphorylation of IKKalpha/beta and I
144 sialylation of TNFR1 had no effect on early TNF-induced signaling events, including the rapid activa
149 ting cytotoxic capacity were increased by F8-TNF plus doxorubicin treatment, arguing that cognate CD8
150 selective splice isoforms of fibronectin (F8-TNF), can be exploited to eradicate sarcomas in immunoco
151 HI-164 fibrosarcoma with a combination of F8-TNF and doxorubicin, curing the majority of treated anim
152 had higher levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6), more neutrophil recruitme
154 OUND & AIMS: Although tumor necrosis factor (TNF) antagonists reduce many clinical features of inflam
157 Dysregulation of tumor necrosis factor (TNF) receptor signaling is a key feature of various infl
158 e driven by increased tumor necrosis factor (TNF) secretion, which leads to activation in turn of c-J
160 rgistic IFN-gamma and tumor necrosis factor (TNF) stimulation promotes strong activation of brain blo
161 Eiger, the only known tumor necrosis factor (TNF) superfamily homolog in Drosophila, Coxiella-infecte
162 ent assays quantified tumor necrosis factor (TNF), interleukin (IL)-12, and IL-10 in gingival tissues
163 AI and inhibition of tumour necrosis factor (TNF), lipopolysaccharide or polyinosinic:polycytidylic a
164 alpha (PPARGC1A), and tumor necrosis factor (TNF), was changed in adipose tissue by overfeeding.
166 terferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-2, but not IL-17A; iii)
168 and the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 in the syno
172 Confirming and extending these findings, TNF, IL-2, and IL-21 also synergistically triggered the
173 1 microM), markedly increase (by 1,000-fold) TNF gene expression in cultured human LAD2 and primary m
174 assays, we show that monocytes deficient for TNF or TNF receptors are outcompeted by their wild-type
175 ry, we found that RARgamma was essential for TNF-induced RIP1-initiated apoptosis and necroptosis.
179 ctivation, develop cutaneous ulceration from TNF exposure, and exhibit severe dextran sodium sulfate-
180 R8-dependent type II interferon (IFN-gamma), TNF-alpha, and IL-12 in myeloid dendritic cells are of i
181 roduction of protective cytokines IFN-gamma, TNF-alpha, and IL-12, as well as recruitment of NK cells
182 ls of the proinflammatory factors IFN-gamma, TNF-alpha, and inducible NO synthase in the TME merely 4
183 y cytokines and chemokines (IL-6, IFN-gamma, TNF-alpha, CXCL1, and CCL2) and extensive splenic damage
184 of the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-1beta and RANTES and activation of p38/Sta
185 educed the expression of inflammatory genes (TNF-alpha, IFN-gamma, IL-1beta, IL-6, and CCL2 mRNAs), a
186 of repeated LPS stimulation in vivo, hepatic TNF-alpha and PCNA responses subsided in Nox4-deficient
187 tory responses (lower IL-10 and CCL2, higher TNF-alpha, IL-6, and IL-1beta) toward pathogenic stimuli
188 e marrow-derived macrophages produced higher TNF-alpha compared with CD44(-/-) macrophages following
191 romoted mucosal secretion of IL-22 and ICOSL/TNF-alpha-dependent release of the IL-22 inducible antim
192 alse discovery rate < 0.05), including IFNG, TNF, CSF2, chemokines, such as CCL3, CCL4, and XCL1, and
195 mpounds 3a, 6b and 7c and found decreases in TNF-alpha and IL-6 release and increase in IL-1beta.
197 vity by proinflammatory cytokines, including TNF, interferes with bone remodeling during inflammation
198 ency in endothelial autophagy also increased TNF-alpha-induced inflammation under high-SS conditions
199 hibitor were protected from diabetes-induced TNF-alpha, IL-1beta, ICAM-1, and NOS2 upregulation.
204 croptosis induced by death receptors ligands TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related
206 n OAs, which could be due to increased local TNF-alpha levels, might lead to impaired eosinophil reso
207 GPx levels in cord blood as well as maternal TNF-alpha levels were inversely associated with maternal
210 n both unadjusted and fully adjusted models: TNF-alpha: hazard ratios (HRs)(1 pg/ml increments), 1.24
211 single injection of picogram amounts of NGR-TNF, a tumor vessel-targeted TNFalpha derivative current
212 or more biological treatments including non-TNF drugs, and 166 (19%) of 878 were not taking a DMARD
213 singly, NK-1 antagonists also inhibit 50% of TNF secretion (P < 0.001) when stimulated only by IL-33,
216 f TRIM28 strikingly suppressed expression of TNF receptor (TNFR)-1 and -2, decreased TNF-alpha-induce
217 hild with HIVAN led to the identification of TNF-alpha as a possible mediator of HIV-1 infection.
219 A against Tnf mRNA reduced protein levels of TNF in colon tissues, compared with mice with colitis gi
220 n coinfected with HIV-1 had higher levels of TNF-alpha and IL-1beta than HIV-uninfected children with
221 ho died in the hospital had higher levels of TNF-alpha, IL-1beta, interleukin 12p70; CCL2, CCL4, CCL1
223 h domain (TRADD) is an essential mediator of TNF receptor signaling, and serves as an adaptor to recr
226 roduction of IL-12 and IFN-gamma, but not of TNF-alpha, IL-6, and IL-8 upon subsequent infection with
228 portant implications for the pathogenesis of TNF-mediated enteropathies and chronic inflammatory dise
229 s identify a unique amplification process of TNF synthesis and secretion via the interaction of NK-1
230 exhibited significantly higher production of TNF and IFNgamma, elevated natural cytotoxicity, and inc
231 of exhaustion, such as reduced production of TNF and IL2 and expression of coinhibitory receptors.
234 Furthermore, the TsSP-induced reduction of TNF secretion from DCs is reversed by receptor antagonis
235 found cIAP1 to be required for regulation of TNF-induced intestinal epithelial cell death and surviva
237 infection, without affecting the release of TNF-alpha, and indicated a role for the inflammasome sen
239 appreciated critical cell-autonomous role of TNF on monocytes for their survival, maintenance, and fu
240 on stem cells was demonstrated by studies of TNF-induced Wnt/beta-catenin target gene expression in m
243 ice revealed that mucosal repair depended on TNF production by BM-derived cells and TNFR expression b
244 of AMPK, ZMP, did not reverse the effects on TNF-alpha-induced CFB expression, suggesting AMPK-indepe
249 we show that monocytes deficient for TNF or TNF receptors are outcompeted by their wild-type counter
250 ytokine production was mediated by paracrine TNF-alpha-TNFR1 signaling rather than direct ligand sens
251 (N-terminal pro-B-type natriuretic peptide), TNF-alpha, IL-6, IL-12, IL-17, malondialdehyde, and fetu
252 irst time, a distinctive role for peripheral TNF-alpha in the modulation of the amyloid phenotype in
255 reatment with glycerophosphoinositol reduced TNF-alpha synthesis, which supports the concept that gly
258 ers stimulated gammadelta T cells to secrete TNF-alpha in response to a variety of tumor cells more e
259 with low-dose LPS resulted in elevated serum TNF levels compared with Nlrp3L351P Casp1/11-/- mice and
261 vels of inflammatory cytokines in the serum (TNF-alpha, IL-6, IL-12, TGF-beta, and VEGF) were down re
264 eptor reduction also decreases SP-stimulated TNF secretion by 30% (P < 0.05), suggesting an interacti
265 y expressed SseK1, SseK2, and SseK3 suppress TNF-alpha-induced, but not Toll-like receptor 4- or inte
272 3 complex to the IL-10 promoter, but not the TNF promoter, thereby tipping the balance towards inflam
275 e Item et al. show that Fas, a member of the TNF receptor superfamily, contributes to mitochondrial d
276 ntributed to identify important roles of the TNF-alpha ligand Eiger and mitogenic molecules in mediat
277 with TNFalpha leads to the formation of the TNF-R1 signaling complex (TNF-RSC) to mediate downstream
279 on, or systemic injections of an antibody to TNF before or during sensitization and challenge phase o
281 nism that regulates the cellular response to TNF and may promote cancer cell survival within TNF-rich
282 ticipates in the proinflammatory response to TNF-alpha, therapeutic strategies targeting this transcr
285 metic compounds (SMCs), sensitize tumours to TNF-alpha-induced killing while simultaneously blocking
286 ukin-1 receptor-associated kinase)1/4-TRAF6 (TNF receptor-associated factor 6), leading to integrin a
287 TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related Apoptosis-Inducing Ligand); is an extremely
289 ]arene-C60, bisporphyrin-trinitrofluorenone (TNF), and Hamilton's bis(acetamidopyridinyl)isophthalami
290 ifferent dimensions, which are released upon TNF-alpha stimulation of endothelial cell cultures.
291 These findings might help to explain why TNF blockade improves lung function in only some patient
292 urthermore, NOSTRIN interacted directly with TNF receptor-associated factor 6 (TRAF6), leading to the
293 r incubation of crypt-derived enteroids with TNF reduced their expression of DRA messenger RNA and pr
296 Stimulation of pulmonary macrophages with TNF-alpha and/or MCP-1 induced expression of both IFN-ga
299 ce, cultured enteroids, incubated these with TNF (50 ng/mL, 24 hours), and quantified messenger RNAs.
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