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1 pression of CD27, and high levels of IgM and IL-6 receptor.
2 ulation and IL-6-induced endocystosis of the IL-6 receptor.
3 f the nonsignaling gp80 alpha-subunit of the IL-6 receptor.
4 only when it was in complex with the soluble IL-6 receptor.
5 gp130, the signal-transducing subunit of the IL-6 receptor.
6 ndothelial cells through a newly constituted IL-6 receptor.
7 on in hepatic cells is equivalent to that of IL-6 receptor.
8 ression of the plasma membrane high-affinity IL-6 receptor.
9 h factor receptor-bound protein 2 (GRB2) and IL-6 receptor.
10 e formation of complexes of IL-6 and soluble IL-6 receptor.
11 increase in the expression of high-affinity IL-6 receptors.
12 ilizumab directed against the interleukin 6 (IL-6) receptor.
15 veral factors, including interleukin (IL)-1, IL-6, receptor activator of NF-kappaB (RANK) ligand, par
17 demonstration of increased expression of the IL-6 receptor after loss of sex steroids provides an exp
18 the non-signaling membrane-bound or soluble IL-6 receptor alpha (IL-6R, sIL-6R), which is referred t
19 ted mice with deletion of the membrane bound IL-6 receptor alpha (IL-6Ralpha) on neural cells, on per
21 nstrate that T cell-specific deletion of the IL-6 receptor alpha chain (IL-6Ralpha) results in impair
22 ignal transducer but is not dependent on the IL-6 receptor alpha subunit (IL-6R, gp80) that is requir
23 reduction in the amount of mRNA encoding the IL-6 receptor alpha subunit and IL-6 binding activity.
24 requirement for transcription is the soluble IL-6 receptor alpha, which translocates to endothelial c
26 n lower expression of the genes encoding the IL-6 receptor alpha-chain (Il6ra) and the IL-6 signal tr
27 nor O-linked glycosylation is necessary for IL-6 receptor alpha-dependent binding to gp130 or signal
28 ot an agonist for this, but we found soluble IL-6 receptor alpha-subunit (IL-6Ralpha), with their con
29 Diminished hepatitis in IL-6-deficient, anti-IL-6 receptor alpha-treated, ovariectomized, or male mic
30 nstruct a model of IL-6 interacting with the IL-6 receptor (alpha-chain) and gp130 (beta-chain) that
33 romal cells acted cooperatively with soluble IL-6 receptor-alpha and thermally induced gp130 to promo
34 r both lymphoid and myeloid fates, expressed IL-6 receptor-alpha chain and responded to IL-6 by phosp
35 scular adhesion were induced by IL-6/soluble IL-6 receptor-alpha fusion protein in mouse tumors and p
36 g pathway, including increased expression of IL-6 receptor-alpha/gp80, activation of the signal trans
37 edly induced mIndy transcription through the IL-6 receptor and activation of the transcription factor
38 F in the peritoneum, do not bear the cognate IL-6 receptor and are thus unable to respond to classic
39 ean winter, with increased levels of soluble IL-6 receptor and C-reactive protein, risk biomarkers fo
40 ction of IL-6 with concomitant expression of IL-6 receptor and gp130 suggest that these factors may p
41 could be rescued by the addition of soluble IL-6 receptor and IL-6 or by retroviral transduction of
42 signaling include antibodies to IL-6 and the IL-6 receptor and inhibitors of janus kinases; several o
43 toplasmic domain of the gp130 subunit of the IL-6 receptor and is different from the SH2 domain-conta
44 omatin, but did not affect the expression of IL-6 receptor and phosphorylation of JAK/STAT3, MAPK, an
45 lassic signaling using the membrane-anchored IL-6 receptor and trans-signaling using its soluble form
46 Here we demonstrate loss of interleukin 6 (IL-6) receptor and IL-6-responsive colony-forming units
47 blotting; however, lower production of both IL-6-receptor and Stat3 explains, in part, reduced activ
48 dothelial cell-derived IL-6 activates IL-6R (IL-6 Receptor) and signal transducer and activator of tr
49 lizumab (TCZ), a monoclonal antibody against IL-6 receptor, and are due in part to the prolongation o
52 s of the gp130 subunit of the interleukin-6 (IL-6) receptor, and a seven amino acid STAT1 recruitment
57 Moderate-to-severe CRS is managed with the IL-6 receptor antagonist tocilizumab with or without cor
59 specific antibodies, IL-12/23 antibodies, an IL-6 receptor antagonist, a sphingosine-1-phosphate agon
60 research questions: (1) Does interleukin 6 (IL-6) (receptor) antagonist therapy reduce mortality in
62 hese data suggest that a randomised trial of IL-6 receptor antagonists in sepsis should be considered
63 to the effect seen in severe COVID-19, where IL-6 receptor antagonists were shown to improve survival
64 de effects in COVID-19 patients treated with IL-6 (receptor) antagonists compared to patients not tre
65 tients compared to patients not treated with IL-6 (receptor) antagonists; and (2) is there an increas
67 as a heterogenous treatment effect with anti-IL-6 receptor antibodies between males and females; with
68 rmeabilized osteoclasts incubated with anti- IL-6 receptor antibodies revealed intense, strictly peri
70 )), whereas in patients who did receive anti-IL-6 receptor antibodies, the risk was lower in males (H
72 d this toxicity was strongly inhibited by an IL-6 receptor antibody (tocilizumab) and less well by TN
73 is study did not reveal any evidence that an IL-6 receptor antibody affects behavioral outcomes in sc
76 : the complement C5 antibody eculizumab, the IL-6 receptor antibody satralizumab, the B cell-depletin
77 Inhibition of IL-6 signaling with the anti-IL-6 receptor antibody tocilizumab has provided some cli
78 interaction between biological sex and anti-IL-6 receptor antibody treatment with respect to hospita
79 ibodies between males and females; with anti-IL-6 receptor antibody use having a greater benefit in p
80 significant interaction between sex and anti-IL-6 receptor antibody use on progression to respiratory
82 purpose of this trial was to test whether an IL-6 receptor antibody, tocilizumab, would improve resid
83 immunosuppression using tocilizumab, an anti-IL-6 receptor antibody, with or without corticosteroids,
84 nt humanized monoclonal antibody against the IL-6 receptor approved for treatment of rheumatoid arthr
85 monoclonal antibodies targeting IL-6 and the IL-6 receptor are also being studied for the management
86 , an anti-inflammatory cytokine, and soluble IL-6 receptor are associated with systemic juvenile rheu
90 RI), IL-1RII, TNF receptor II (TNFR II), and IL-6 receptor as well as the level of proinflammatory cy
92 was associated with a 2-4-fold reduction of IL-6 receptor at protein and mRNA levels in SGN-40-treat
94 desensitization strategies, the addition of IL-6 receptor blockade resulted in desensitization with
95 e and immunoabsorption as well as subsequent IL-6 receptor blockade through tocilizumab, a complete a
96 sults from the recent clinical studies using IL-6 receptor blockade, and describe potential mechanism
101 but failed to affect the mRNA expression of IL-6 receptor chains or activation of JAK2 and STAT3.
102 Furthermore, cholangiocytes possessed the IL-6 receptor complex subunits and intact signaling mech
106 gnaling driven by CD4 T cell-derived soluble IL-6 receptor complexed with fibroblast-derived IL-6 pro
107 ditional knockout (cKO) model with selective IL-6 receptor deletion in T cells (IL-6R-cKO), we demons
109 ies against IL-6 or the gp130 subunit of the IL-6 receptor did not attenuate ET-1-induced collagen ac
114 al practice by immunotherapy that blocks the IL-6 receptor encoded by IL6R We describe two patients w
120 tentiation is likely due to the induction of IL-6-receptor expression as well as prolonged intensity
121 uingly, IL-6 trans-signaling via the soluble IL-6 receptor, facilitated by elevated levels of IL-6, a
122 esses targeting plasma cell and interleukin (IL)-6 receptor for desensitization in a sensitized nonhu
123 (vIL-6), which does not require the cellular IL-6 receptor for binding to the ubiquitously expressed
125 leotide polymorphisms (SNPs) in and near the IL-6 receptor gene (IL6R), including the non-synonymous
126 ion results in the induction of the IL-6 and IL-6 receptor genes and neutralizing antibodies directed
127 l effect of inflammatory markers (CRP, IL-6, IL-6 receptor, GlycA) on the cognitive functions examine
128 RNA of the signal-transducing subunit of the IL-6 receptor (gp130) in cells of the bone marrow stroma
129 ted by the signal-transducing subunit of the IL-6 receptor, gp130, or by co-transfected IL-3 receptor
131 data suggest tissue-specific differences in IL-6-receptor-gp130-coupled signaling, thereby limiting
133 Stem-like and progenitor cells expressed the IL-6 receptor gp80 with concomitant expression of pSTAT3
134 dence that the ligand-binding subunit of the IL-6 receptor (gp80) is a limiting factor for the action
137 s have been observed in association with the IL-6 receptor; however, inhibition of Src kinases by Csk
141 kin-6 (IL-6) trans-signaling via the soluble IL-6 receptor (IL-6R) and robustly support adult neuroge
142 ynthesis of interleukin-6 (IL-6) and soluble IL-6 receptor (IL-6R) and stimulated Janus kinase-2 (JAK
144 liminary results have been obtained with the IL-6 receptor (IL-6R) antagonist tocilizumab for the tre
146 L-6 can mediate proinflammatory effects, and IL-6 receptor (IL-6R) blockade as a treatment for inflam
147 The current study evaluated the effect of IL-6 receptor (IL-6R) blockade with an antiYIL-6R monocl
148 ly competes for binding to the cytokine with IL-6 receptor (IL-6R) by using side chains of two CDR re
149 DC-driven classical signaling after targeted IL-6 receptor (IL-6R) deletion in T cells eliminated pat
150 FN-alpha growth-inhibited cell lines reduced IL-6 receptor (IL-6R) expression, IFN-alpha also reduced
153 d by membrane-bound and soluble forms of the IL-6 receptor (IL-6R) in processes called classic and tr
154 atitis has been reported after initiation of IL-6 receptor (IL-6R) inhibitors (IL-6Ri), while genetic
155 by way of antibody-mediated blockade of the IL-6 receptor (IL-6R) markedly reduces pathologic damage
156 ession in the normal liver, but both met and IL-6 receptor (IL-6R) mRNA are detectable; met mRNA is e
160 efined, nor has the behavior of the specific IL-6 receptor (IL-6R) or the signal transducer gp130.
161 a receptor complex consisting of the cognate IL-6 receptor (IL-6R) or the soluble IL-6 receptor (sIL-
165 wth factor (IGF)/IGF-1 receptor (IGF-1R) and IL-6 receptor (IL-6R) signaling cascades, antiapoptotic
166 -regulation and crosstalk of the AMR and the IL-6 receptor (IL-6R) to induce JAK2-STAT3-TPO activatio
168 : classical signaling via its membrane-bound IL-6 receptor (IL-6R), and trans-signaling via a natural
169 e clinical usage of monoclonal antibodies to IL-6 receptor (IL-6R), designed to block IL-6 pathways.
170 would interact with the specific alpha-chain IL-6 receptor (IL-6R), is accessible and not occupied by
173 pilot study of DES using a novel drug (anti-IL-6 receptor (IL-6R),Tocilizumab [TCZ]) + intravenous I
174 tocytes also do not show activation of other IL-6 receptor (IL-6R)-mediated Janus kinase substrates,
176 xamer, formed by the association of two IL-6.IL-6 receptor (IL-6R).gp130 trimers, with gp130 being th
177 nction in 2 ways: by directly binding to the IL-6 receptor (IL-6R; CD126) or via trans-signaling, in
178 is not dependent on the structurally related IL-6 receptor (IL-6R; gp80) subunit of the receptor-sign
179 signaling) or soluble (trans-signaling; TS) IL-6 receptors (IL-6Rs) to regulate liver injury respons
180 hybridoma cell line, B9, and that the gp80 (IL-6 receptor [IL-6R]) component of the IL-6 receptor-si
182 a role in cytokine signaling, including the IL-6 receptor, IL-1 receptor type I, and IL-1 receptor t
183 an ability of interferon-alpha and a soluble IL-6 receptor/IL-6 (sIL-6R alpha/IL-6) trans-signaling c
185 elated common variants in the interleukin-6 (Il-6) receptor (IL6R) gene to plasma C-reactive protein
186 ack loops, in part by directly targeting the IL-6 receptor (IL6RA) gene, and, thus, amplifying IL-6 a
187 We demonstrate a higher ratio of SOCS3 to IL-6 receptor in adult monocytes than in fetal monocytes
189 ting OXPHOS in the young TME or blocking the IL-6 receptor in the aged TME reduces the age-specific p
190 ially due to increased expression of soluble IL-6 receptor in the brain relative to the spinal cord t
191 Neutralizing autocrine IL-6 and/or blocking IL-6 receptors in IL-6(+)/gp80(+) MCL cells inhibited ce
192 humanised monoclonal antibody targeting the IL-6 receptor, in patients with generalised myasthenia g
193 ther oncostatin M (OSM) or IL-6 plus soluble IL-6 receptor increased the levels of p21 mRNA and prote
194 we hypothesised that, in these patients, the IL-6 receptor inhibitor tocilizumab would be more effect
195 found that these cells synthesized IL-6 and IL-6 receptors; interruption of this pathway by IL-6 ant
199 lobal IL-1 receptor gene knockout or central IL-6 receptor knockdown showed attenuated decrease in fo
202 ncrease: 2.3, 1.4-3.8, P = .001) and soluble IL-6 receptor level was associated within 6 years after
203 ptin binding and responded to leptin with an IL-6 receptor-like signaling that includes the activatio
204 these studies suggest that blocking IL-1 or IL-6 receptors may improve the regenerative capacity of
209 se transcriptase-PCR analysis indicated that IL-6 receptor mRNA was present in all carcinoma cell lin
210 6 showed a significant reduction in IL-6 and IL-6 receptor mRNA, together with significant decreases
211 sed to study the effects of dexamethasone on IL-6 receptor number in the well-differentiated human he
213 Activated T cells expressed lower levels of IL-6 receptors on their surfaces, yet there were suffici
214 rs (CRP, GlycA, IL-6, IL-6 receptor, soluble IL-6 receptor) on cognitive measures (above) and on gene
215 clast formation stimulated by IL-6 + soluble IL-6 receptor, oncostatin M, or IL-1 but not by parathyr
217 mor necrosis factor (TNF) and interleukin-6 (IL-6) receptor, only 20 to 30% of patients experience re
222 y receptor-mediated (i.e., TNFalpha, NGF, or IL-6 receptor) or direct activation of protein kinase Ce
223 ceptor IL-6R (sIL-6R); by an antibody to the IL-6 receptor; or by minocycline, which inhibits the mic
224 NP mendelian randomisation using increase in IL-6 receptor plasma protein as an exposure revealed a s
226 examined change in the ratio of IL-6:soluble IL-6 receptor pre-intervention, post-intervention, and a
228 DL1-mediated reduction in membrane (m)-bound IL-6 receptor (R) expression, converting progenitor cell
229 deling tested whether increased IL-6:soluble IL-6 receptor ratio post-intervention was associated wit
230 hyperthermia only increased the IL-6:soluble IL-6 receptor ratio post-treatment [F(3,72) = 11.73,p <
231 d 6, such that increases in the IL-6:soluble IL-6 receptor ratio were associated with decreased depre
232 hich blocks leukocyte TNF, TNF receptor, and IL-6 receptor release, also inhibits L-selectin shedding
233 dependently of the gp80 alpha-subunit of the IL-6 receptor, required for hIL-6 signal transduction.
236 aft proteins caveolin-1 and flotillin-1, the IL-6-receptor signal transducing chain gp130, the interf
237 p80 (IL-6 receptor [IL-6R]) component of the IL-6 receptor-signal transducer (gp180) complex plays a
238 al protein S6 kinase, respectively) and IL-6/IL-6 receptor signaling (i.e., IL-6 production and signa
242 dentify TRAF5 as a negative regulator of the IL-6 receptor signaling pathway that limits the inductio
247 o investigate the role of the interleukin 6 (IL-6) receptor signaling in the pathogenesis of MCD and
249 lpha (TNFalpha) and the soluble interleukin (IL)-6 receptor (sIL-6R), the latter of which drives proi
250 though treatment with either IL-6 or soluble IL-6 receptor (sIL-6R) alone had no effect on VEGF produ
251 cognate IL-6 receptor (IL-6R) or the soluble IL-6 receptor (sIL-6R) and glycoprotein 130 (gp130).
253 tagonist of the interleukin-6 (IL-6)/soluble IL-6 receptor (sIL-6R) complex and selectively inhibits
256 pproximately twofold higher IL-6 and soluble IL-6 receptor (sIL-6R) levels compared to matched pre-CL
257 s to evaluate the effect of IL-6 and soluble IL-6 receptor (sIL-6R) on hematopoietic and skeletal act
259 forms an agonistic complex with the soluble IL-6 receptor (sIL-6R) to activate all cells expressing
260 studies link high levels of IL-6 and soluble IL-6 receptor (sIL-6R) to asthma severity and decreased
261 al fibroblasts treated with IL-6 and soluble IL-6 receptor (sIL-6R) was used to probe a cytokine micr
262 hanced through transsignaling by the soluble IL-6 receptor (sIL-6r), allowing for the pleiotropic cyt
263 liver enzymes, interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and soluble tumor necrosis facto
264 d respond to IL-6 in the presence of soluble IL-6 receptor (sIL-6R), but the cell surface expression
265 Expression of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), IL-10, and IL-13 was detected by
266 production of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), IL-10, and tumor necrosis factor
271 xied inflammatory markers (CRP, GlycA, IL-6, IL-6 receptor, soluble IL-6 receptor) on cognitive measu
272 ore, suppression of Il6ra, the gene encoding IL-6 receptor, specifically in AP neurons with CRISPR/dC
273 dium of cytokine (TNF-alpha and IL-6/soluble IL-6 receptor)-stimulated human cartilage explants.
274 athecal treatment with antisense directed to IL-6 receptor subunit gp130 (gp130), but not to tumor ne
275 in the endothelium for the expression of the IL-6 receptor subunit, IL-6 signal transducer (IL6ST; gp
276 with colitis was increased 80-fold, and the IL-6 receptor subunits IL-6R alpha and gp130 were presen
279 b (TCZ) is a humanized monoclonal anti-human IL-6 receptor that inhibits IL-6-mediated proinflammator
280 26 variants in the gene encoding the IL-6R (IL-6 receptor) that proxied for pharmacological IL-6R in
282 Moreover, addition of soluble interleukin-6 (IL-6) receptor to the medium endowed IL-6 with the abili
283 onal antibodies against CD20 (rituximab) and IL-6 receptor (tocilizumab), the latter also in clinical
284 ane-bound (classic signaling) or the soluble IL-6 receptor (trans-signaling), we first performed cell
286 i-IL-6 IMB was far superior to systemic anti-IL-6 receptor treatment in prolonging skin allograft sur
287 pression of IL-6 in combination with soluble IL-6 receptor was a reliable predictor of ALI in SAP.
289 SHV-positive plasmablasts, whereas the human IL-6 receptor was expressed in most KSHV-positive cells.
291 s phosphorylated after IL-6 binding to gp80 (IL-6 receptor), we hypothesized that gp130 could be invo
292 1 and 2), as well as interleukin (IL)-6 and IL-6 receptor were measured on a daily, weekly and month
294 well as signaled by increased pSTAT3 via the IL-6 receptor, which inhibits IRS 1/2 phosphorylation.