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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.
13  IL-6 effect was abrogated by excess soluble IL-6 receptor (500 microg/l).
14 6 were mediated by complexation with soluble IL-6 receptor, a process known as trans-signaling.
15 veral factors, including interleukin (IL)-1, IL-6, receptor activator of NF-kappaB (RANK) ligand, par
16                  PAC inhibits interleukin 6 (IL-6) receptor activity and pathogenic T helper cell 1 (
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
20                  The association of IL-6 and IL-6 receptor alpha (IL-6Ralpha) with asthma was reporte
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
25                                  Using their IL-6 receptor alpha-chain (IL-6Ralpha), Sirpalpha(+) DCs
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
31                       The interleukin (IL)-6/IL-6 receptor-alpha (IL-6Ralpha)/signal transduction and
32 cing chain by IL-6 and a soluble form of the IL-6 receptor-alpha (sIL-6Ralpha) binding subunit.
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
50          The OPC cell lines used express the IL-6 receptor, and IL-6 stimulation of these cells cause
51                                        IL-6, IL-6 receptor, and phospho-signal transducer and activat
52 s of the gp130 subunit of the interleukin-6 (IL-6) receptor, and a seven amino acid STAT1 recruitment
53 d soluble IL-1 receptor II; IL-6 and soluble IL-6 receptor; and IL-10.
54 nhibition (atacicept) and IL-6 as opposed to IL-6 receptor antagonism, have also been evaluated.
55                                          The IL-6 receptor antagonist tocilizumab could potentially d
56                            Rapamycin and the IL-6 receptor antagonist Tocilizumab reduce alveolar typ
57   Moderate-to-severe CRS is managed with the IL-6 receptor antagonist tocilizumab with or without cor
58 cytokine in the toxicity response, using the IL-6 receptor antagonist tocilizumab.
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
61 ding later confirmed in randomised trials of IL-6 receptor antagonists (IL6RAs).
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
66 onists compared to patients not treated with IL-6 (receptor) antagonists?
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
69        For patients who did not receive anti-IL-6 receptor antibodies, the risk of death was slightly
70 )), whereas in patients who did receive anti-IL-6 receptor antibodies, the risk was lower in males (H
71 of which 58% were male and 15% received anti-IL-6 receptor antibodies.
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
74 gration when added to uninfected HPNCs; anti-IL-6 receptor antibody prevented these changes.
75                         Importantly, an anti-IL-6 receptor antibody prevented virus-induced perineuri
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
81              Rationale: Tocilizumab, an anti-IL-6 receptor antibody, had no statistically significant
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
87                                 We show that IL-6 receptors are present in intestinal epithelia in a
88                                              IL-6 receptors are present on pituitary corticotrophs an
89  effect required NGF or NT-3 but not soluble IL-6 receptor as cofactors.
90 RI), IL-1RII, TNF receptor II (TNFR II), and IL-6 receptor as well as the level of proinflammatory cy
91 that sex steroids regulate expression of the IL-6 receptor as well.
92  was associated with a 2-4-fold reduction of IL-6 receptor at protein and mRNA levels in SGN-40-treat
93 neutralizing antibodies directed against the IL-6 receptor block Rac1-induced STAT3 activation.
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
97 ar1(-/-)) or by combining anti-PD-1 and anti-IL-6-receptor blockade.
98 he IL-1 receptor antagonist anakinra and the IL-6 receptor blocker tocilizumab.
99 uppressive function on the expression of the IL-6 receptor by T cells.
100 eptor signaling complexes with the synthetic IL-6 receptor chain SyCyR(gp130).
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
103 e the nonsignaling gp80 alpha subunit of the IL-6 receptor complex.
104 ecifically mediated by signaling through the IL-6 receptor complex.
105 equential assembly of a functional hexameric IL-6 receptor complex.
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
108                                Inhibition of IL-6 receptor demonstrated to reduce periodontal inflamm
109 ies against IL-6 or the gp130 subunit of the IL-6 receptor did not attenuate ET-1-induced collagen ac
110 mab; however, he had rapid improvement after IL-6 receptor-directed therapy with tocilizumab.
111                                    Since the IL-6 receptor does not contain binding sites for the p85
112         Anti-IL-6 antibodies or blocking the IL-6 receptors elicits reduced collagen synthesis, sugge
113                        Here, we devised anti-IL-6 receptor eluting gelatin methacryloyl (GelMA) bioma
114 al practice by immunotherapy that blocks the IL-6 receptor encoded by IL6R We describe two patients w
115 e found that IL-2 and TGF-beta down-regulate IL-6 receptor expression and IL-6 signaling.
116                                              IL-6 receptor expression in single osteoclasts was confi
117 ediated increases in transport by increasing IL-6 receptor expression on the cell surface.
118 roliferative disorders, viral IL-6 and human IL-6 receptor expression was examined.
119 ne representing the only site of unequivocal IL-6 receptor expression.
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
124                   Treating mice with soluble IL-6 receptor fusion protein or silencing STAT3 in tumor
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
130                             By circumventing IL-6-receptor-gp130-coupled signaling with ectopic expre
131  data suggest tissue-specific differences in IL-6-receptor-gp130-coupled signaling, thereby limiting
132                    We determined the role of IL-6-receptor-gp130-Stat3 signaling in IL-6 activation o
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
135  effect because IFN-alpha down-regulates the IL-6 receptor, gp80.
136  a humanized monoclonal antibody against the IL-6 receptor, has shown an excellent response.
137 s have been observed in association with the IL-6 receptor; however, inhibition of Src kinases by Csk
138        A functional amino acid change in the IL-6 receptor (IL-6R Asp358Ala; rs2228145) was significa
139 itigated by a common germline variant of the IL-6 receptor (IL-6R p.D358A).
140                           An antibody to the IL-6 receptor (IL-6R) alpha subunit effectively neutrali
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
143             Key substrates of ADAM17 are the IL-6 receptor (IL-6R) and TNF-alpha.
144 liminary results have been obtained with the IL-6 receptor (IL-6R) antagonist tocilizumab for the tre
145 e expression of major components of the IL-6/IL-6 receptor (IL-6R) axis.
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
151                             A variant in the IL-6 receptor (IL-6R) gene increases asthma risk and is
152                   New therapies blocking the IL-6 receptor (IL-6R) have recently become available and
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
157 atibility between host rodent IL-6 and human IL-6 receptor (IL-6R) on donor hepatocytes.
158                                 Mice lacking IL-6 receptor (IL-6R) or IL-1 receptor 1 (IL-1R1) specif
159         Moreover, antibodies specific to the IL-6 receptor (IL-6R) or the gp130 subunit were capable
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-
162                         Interleukin-6 (IL-6)/IL-6 receptor (IL-6R) plays a major role in autocrine/pa
163            This IL6R coding change increases IL-6 receptor (IL-6R) shedding and promotes IL-6 transsi
164 and Th17 polarization requires an additional IL-6 receptor (IL-6R) signal.
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
167  monoclonal antibodies directed at IL-6, the IL-6 receptor (IL-6R), and Janus kinase inhibitors.
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
171                          Expression of IL-6, IL-6 receptor (IL-6R), or glycoprotein 130, as well as I
172               Furthermore, we identified the IL-6 receptor (IL-6R), which mediates IL-6-dependent STA
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,
175 d, signal-transducing receptor gp130 and the IL-6 receptor (IL-6R).
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
181             Among these is tocilizumab (anti-IL-6 receptor [IL-6R]) which holds promise for modulatin
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
184 ited adipocyte IL-6 expression and IL-6 plus IL-6 receptor (IL6R) in myocytes and blood.
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
188 orms a complex with the gp130 subunit of the IL-6 receptor in an IL-6-dependent manner.
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
196                  The increased expression of IL-6 receptor is correlated with increased proliferation
197                         The concentration of IL-6 receptor is increased eightfold in the prostate can
198                             Signaling by the IL-6 receptor is mediated through the signal transducing
199 lobal IL-1 receptor gene knockout or central IL-6 receptor knockdown showed attenuated decrease in fo
200 st AILI was abolished in hepatocyte-specific IL-6 receptor knockout mice.
201                 Importantly, blockade of the IL-6 receptor led to diminished swelling of a control CH
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
205                    We hypothesised that anti-IL-6 receptor monoclonal antibodies are associated with
206 S) treated with the anti-interleukin-6 (anti-IL-6) receptor monoclonal antibody tocilizumab.
207                     Interleukin-6 (IL-6) and IL-6 receptor mRNA and protein have been reported in dif
208                                   Similarly, IL-6 receptor mRNA histostaining was increased in osteoc
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
212                            Neutralization of IL-6 receptor on ECs abolished the ability of HCMV secre
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
216           This explains why mice lacking the IL-6 receptor only in osteoblasts exhibit a deficit in e
217 mor necrosis factor (TNF) and interleukin-6 (IL-6) receptor, only 20 to 30% of patients experience re
218                  Either a blocking Ab to the IL-6 receptor or a neutralizing Ab to IL-6 significantly
219 blocked the ability of either IL-6 + soluble IL-6 receptor or oncostatin M to induce RANKL.
220          Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of I
221                                 Blocking the IL-6 receptor or the C5 complement pathway reduces relap
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
225 cestry-specific, multiple SNP approach using IL-6 receptor plasma protein as an exposure.
226 examined change in the ratio of IL-6:soluble IL-6 receptor pre-intervention, post-intervention, and a
227       It is likely that this upregulation of IL-6 receptors "primes" human liver cells for subsequent
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.
234                   The level of soluble human IL-6 receptor (shuIL-6R) in murine serum and fluorescenc
235          STAT3 serves as the mediator of the IL-6 receptor signal and appears to contribute to the tr
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
239                                     Blocking IL-6 receptor signaling from Janus kinases to the Stat3
240 at there is activation-induced inhibition of IL-6 receptor signaling in T cells.
241                            Activation of the IL-6 receptor signaling pathway may play a role in diffe
242 dentify TRAF5 as a negative regulator of the IL-6 receptor signaling pathway that limits the inductio
243 ory responses, its role in the regulation of IL-6 receptor signaling remains unclear.
244 ignaling-3 (SOCS-3), a negative regulator of IL-6 receptor signaling.
245 lls from SKGNur mice were hyperresponsive to IL-6 receptor signaling.
246 or and are thus unable to respond to classic IL-6 receptor signaling.
247 o investigate the role of the interleukin 6 (IL-6) receptor signaling in the pathogenesis of MCD and
248 c activation of STAT3 by T-cell receptor and IL-6 receptor signals.
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).
252                         Soluble forms of the IL-6 receptor (sIL-6R) bind to the cytokine IL-6 with si
253 tagonist of the interleukin-6 (IL-6)/soluble IL-6 receptor (sIL-6R) complex and selectively inhibits
254                             IL-6 and soluble IL-6 receptor (sIL-6R) expression in induced sputum of a
255 ession; however, the addition of the soluble IL-6 receptor (sIL-6R) induced IL-6 transcripts.
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
258                        Surprisingly, soluble IL-6 receptor (sIL-6R) produced initial decrease of sEPS
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
267 oteases and receptors, including the soluble IL-6 receptor (sIL-6R), were then quantitated.
268 d secreted significant levels of the soluble IL-6 receptor (sIL-6R).
269 -6 alone and in combination with the soluble IL-6 receptor (sIL-6R).
270  secretion of interleukin (IL)-6 and soluble-IL-6 receptor (sIL-6R).
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
277    Patients with genetic deficiencies of the IL-6 receptor suffer from "hyper IgE syndrome."
278 enhanced effects observed when combined with IL-6 receptor targeting.
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
281        To mark the tenth anniversary of anti-IL-6 receptor therapy worldwide, we discuss the history
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
285 hagy in myotubes when complexed with soluble IL-6 receptor (trans-signaling).
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.
288 s depleted from MSC conditioned media or the IL-6 receptor was blocked on tumor cells.
289 SHV-positive plasmablasts, whereas the human IL-6 receptor was expressed in most KSHV-positive cells.
290       Immunolabeling studies showed that the IL-6 receptor was restricted to the basal membrane of Pa
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
293 recruits microglial cells to provide soluble IL-6 receptor, which can form complexes with IL-6.
294 well as signaled by increased pSTAT3 via the IL-6 receptor, which inhibits IRS 1/2 phosphorylation.

 
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