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1 Instead, it is determined by competition for interleukins.
4 h their role in Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) mediated signaling pathwa
5 ctivate downstream signaling via TIRAP (Toll-interleukin 1 receptor domain containing adaptor protein
6 ic brain injury, and to evaluate the role of interleukin-1 (IL-1) signaling as a target for pharmacol
7 DCs are defined by their ability to release interleukin-1 (IL-1) while maintaining cell viability, e
10 lammatory mediators include cytokines of the interleukin-1 family, such as IL-1alpha and IL-1beta.
11 members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signal
12 esponses by targeted degradation of the Toll/interleukin-1 receptor (TIR) domain-containing adaptor p
14 culating levels of C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra), and soluble
15 py efficacy stemmed from the upregulation of interleukin-1 receptor antagonist and suppression of MDS
16 chemoattractant protein-1, resistin, soluble interleukin-1 receptor I, soluble interleukin-2 receptor
18 pathway involving the MyD88 adapter and the interleukin-1 receptor-associated kinase (IRAK) complex.
19 main containing adaptor protein)-MyD88-IRAK (interleukin-1 receptor-associated kinase)1/4-TRAF6 (TNF
20 ide primarily protects mice by repressing an interleukin-1- and 12/15-lipoxygenase-dependent neutroph
25 creened the gamma interferon (IFN-gamma) and interleukin-10 (IL-10) responses to 6 HCMV peptide pools
29 consisting of interleukin-6, interleukin-8, interleukin-10, and fractalkine was identified to be the
30 and 3) selective secretion of interleukin-6, interleukin-10, and vascular endothelial growth factor t
31 egulatory B-cell-associated surface markers, interleukin-10, chemokine receptors, and immunoglobulin
32 application, secreting human proinsulin and interleukin-10, cured 66% of mice with new-onset diabete
34 bdaR1 subunit, specific for IFN-lambdas, and interleukin-10Rbeta (IL-10Rbeta), which is shared by mul
37 ever, inborn errors in STAT4, which controls interleukin-12 (IL-12) responses, have not yet been repo
38 binds the p40 subunit of interleukin-23 and interleukin-12 and thereby blocks the activity of these
39 al had higher levels of TNF-alpha, IL-1beta, interleukin 12p70; CCL2, CCL4, CCL13, CCL17, CXCL8, CXCL
40 ory cytokines (interleukin-3, interleukin-6, interleukin-13, interleukin-17, macrophage inflammatory
45 nce of small airway abnormality on CT, lower interleukin-15 concentrations, and higher interleukin-8
47 after HSCT and favored by the high levels of interleukin-15 present in patients' sera, immature NK ce
48 ence of caspase-3 activity of hepatocellular interleukin 16 (IL-16) is no longer processed and releas
49 are: Interferon Stimulated Gene 15 (ISG15), Interleukin 16 (IL16), 2',5'-Oligoadenylate Synthetase L
51 reflected by heightened interferon gamma and interleukin 17 (IL-17) production as well as by high lev
52 ith ex vivo screening, and was essential for interleukin-17 A (IL-17A)-mediated cross-reactivity and
53 cells was seen with increased expression of interleukin-17 and interleukin-22 by day 5 after injury.
55 nterleukin-3, interleukin-6, interleukin-13, interleukin-17, macrophage inflammatory proteins-1alpha,
57 at we detected had an increased frequency of interleukin 17A production compared with responses of T
58 tear levels of the proinflammatory cytokine interleukin 17A were significantly reduced in the krill
60 Th1 and Th17 cytokines interferon-gamma and interleukin 17A, and are unresponsive to in vitro PD-1 b
62 tection was associated with the induction of interleukin-17A (IL-17A), IL-22, and gamma interferon (I
63 trinsic role in promoting both IFN-gamma and interleukin-17A production during infection with C. rode
64 -) mice were given injections of recombinant interleukin 18 (rIL18) or saline (control) during DSS ad
65 MAIT cells was dependent on monocyte-derived interleukin 18, and was reduced in patients with HCV inf
69 nterleukin-6, interleukin-8, interleukin-10, interleukin-18, and tumor necrosis factor-R2 were each s
70 o immunomodulatory therapeutics.The cytokine interleukin 1alpha (IL-1alpha) plays an important role i
75 gnificant difference was detected: Levels of interleukin 1beta (IL-1beta) were lower in dengue-infect
77 nal tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta), intracellular adhesion mol
78 es (controls) and analyzed expression NLRP3, interleukin 1beta (IL1B, in plasma), and IL18 (in plasma
79 riate analyses adjusting for covariates IL6, interleukin 1beta (IL1beta), and interleukin 1Ralpha (IL
80 active protein (CRP), tumor necrosis factor, interleukin 1beta, 6, and 10, leukocyte telomere length,
81 roinflammatory cytokines (eg, interleukin 6, interleukin 1beta, and tumor necrosis factor alpha) in c
82 (qRT-PCR), and the proinflammatory cytokines interleukin 1beta, interferon beta, and RANTES (regulate
83 ealed increased transcriptional induction of interleukin 1beta, interferon beta, and RANTES in ZIKV-i
84 e CNS, Rag1(-/-) mice showed lower levels of interleukin 1beta, reduced microglial proliferation, and
85 atory (NLR family pyrin domain containing 3, interleukins 1beta and 6, and cysteine-cysteine chemokin
88 There is a strong link between integrins and interleukin-1beta (IL-1beta), but the specifics of the r
90 nal immunopathology (neutrophil recruitment, interleukin-1beta [IL-1beta] secretion, and lactate dehy
91 vity was evaluated by measuring the level of interleukin-1beta and -18 in the supernatants of activat
92 eased concentrations of active caspase-1 and interleukin-1beta are related to an increased concentrat
93 1- and CD3-positive cells, the production of interleukin-1beta by CD11b- and Iba-1-positive cells, an
95 its release of the pro-inflammatory cytokine interleukin-1beta from activated microglia, consistent w
97 (CANTOS), a randomised trial of the role of interleukin-1beta inhibition in atherosclerosis, with th
98 roptosis, as measured by caspase-1-dependent interleukin-1beta release, though this phenotype could b
100 expression, caspase 1 activity, or IL-1beta (interleukin-1beta) protein expression under in vivo and
101 cytokines/chemokines in the brain, including interleukin-1beta, interferon-gamma, and fractalkine as
102 ZDF islets contain elevated levels of CB1R, interleukin-1beta, tumor necrosis factor-alpha, the chem
104 riates IL6, interleukin 1beta (IL1beta), and interleukin 1Ralpha (IL1Ralpha) were associated with inc
107 or [gammadelta-TCR]) and cytokines examined (interleukin 2 [IL-2], IL-4, IL-10, IL-17A, and gamma int
109 CCL2, CCL4, CCL13, CCL17, CXCL8, CXCL10; and interleukin 2 and interferon gamma than children who sur
110 and CD8+ T cells and a higher proportion of interleukin 2-secreting cells (P = .01 and P = .002, res
111 compared to CD8(+) T cells) that coexpressed interleukin-2 (IL-2) (66.4%) and/or tumor necrosis facto
116 n, soluble interleukin-1 receptor I, soluble interleukin-2 receptor alpha, and tumor necrosis factor
117 tandard induction immunosuppression was with interleukin-2 receptor antagonists, and antithymocyte gl
118 PREX1-Rac1-signaling pathway that stabilizes interleukin-2(IL-2), IL-4, and IL-10 messenger RNA (mRNA
120 efficacy of CD20-targeted therapy, we fused interleukin 21 (IL-21), which induces direct lymphoma cy
121 se 1 dose-escalation study of membrane-bound interleukin 21 (mbIL21) expanded donor NK cells infused
122 ), CD4+IL17A+ cells (P < .01), and CD4+CXCR5+interleukin 21+ follicular T-helper (Tfh) cells (P < .01
123 found that a small subset of gp120-specific interleukin-21 (IL-21)-secreting CXCR5(+) CD4(+) T cells
128 g HFD with inulin restored microbiota loads, interleukin-22 (IL-22) production, enterocyte proliferat
131 onoclonal antibody that selectively inhibits interleukin 23 (IL23), a cytokine implicated in the path
132 ty, humanised, IgG1 kappa antibody targeting interleukin 23 p19 that represents an evolving treatment
133 t dominates the binding affinity for an anti-interleukin-23 (anti-IL-23) antibody by using the comple
135 b, an antibody that binds the p40 subunit of interleukin-23 and interleukin-12 and thereby blocks the
139 In this phase 2 trial, selective blockade of interleukin-23 with risankizumab was associated with cli
140 the activity of these cytokines, inhibiting interleukin-23-dependent production of interleukin-17.
141 show that BST-2 upregulation by IFN-beta and interleukin-27 (IL-27) also increases the surface expres
142 egulatory T cells (Tr1 cells) are induced by interleukin-27 (IL-27) and have critical roles in the co
144 is demonstrate that plasma levels of soluble interleukin-27 (IL-27) are significantly elevated in ind
145 , we show that the immunoregulatory cytokine interleukin-27 is upregulated centrally and peripherally
148 c-kit mutant Kit(W/W-v) mice indicated that interleukin-3 and c-Kit contribute to expulsion of the i
149 with transgenic expression of human GM-CSF, interleukin-3, and stem cell factor in a NOD/SCID-IL2Rga
150 ced production of proinflammatory cytokines (interleukin-3, interleukin-6, interleukin-13, interleuki
151 ibe a type 2 immune circuit where pancreatic interleukin-33 (IL-33) promotes insulin secretion via th
152 lammation (interleukin-6, interleukin-8, and interleukin-33 and soluble suppression of tumorigenicity
153 ipient microbiome, the impact of the alarmin interleukin-33 on alloreactivity, and the role of Notch
155 ngiopoietin-2, interleukin-6, interleukin-8, interleukin-33, and soluble suppression of tumorigenicit
156 T cells, we show that FLIL33, but not mature interleukin-33, physically interacts with IPO5 and that
159 was associated with exposure, with increased interleukin-4 (IL-4) production, IL-5 transcription, and
161 ergy expenditure in wild-type, Ucp1(-/-) and interleukin-4 receptor-alpha double-negative (Il4ra(-/-)
165 Benralizumab is an anti-eosinophilic, anti-interleukin-5 receptor alpha monoclonal antibody that ha
166 dy directed against the alpha subunit of the interleukin-5 receptor that significantly reduces the in
168 ological mechanical damage, via induction of interleukin 6 (IL-6) from epithelial cells, tailored eff
169 describe a new mouse strain, in which human interleukin 6 (IL-6) gene encoding the cytokine that is
171 ding protein (I-FABP), soluble CD14 (sCD14), interleukin 6 (IL-6), and C-reactive protein (CRP) at 6
173 re; Egfr(f/f) mice had reduced expression of interleukin 6 (IL6), and epithelial STAT3 activation was
174 ripheral blood mononuclear cells and reduced interleukin 6 (P = .028) and GVHD biomarkers (Reg3, P =
175 red parasite biomass, systemic inflammation (interleukin 6 [IL-6]), endothelial activation (angiopoie
176 pondin 2; intercellular adhesion molecule 1; interleukin 6 [IL-6]; stromal cell-derived factor 1; tis
177 ssociated among HIV-infected men with higher interleukin 6 and high-sensitivity C-reactive protein an
180 D5Rs (DRD5KO mice) to show that carrageenan, interleukin 6, as well as BDNF-induced hyperalgesia and
181 The following measurements were obtained: interleukin 6, high-sensitivity C-reactive protein, solu
182 ed SAMHD1 and proinflammatory cytokines (eg, interleukin 6, interleukin 1beta, and tumor necrosis fac
190 pendent on exogenous soluble factors such as interleukin-6 (IL-6) and APRIL, to prevent their cell de
193 erclonal communication mechanism mediated by interleukin-6 (IL-6) cytokine secreted from EGFRvIII-pos
194 ilage explants, suppressing pro-inflammatory interleukin-6 (IL-6) expression after interleukin-1 beta
196 used infiltration of the peripheral cytokine interleukin-6 (IL-6) into brain parenchyma and subsequen
197 ons of FITC-dextran gut translocation, serum interleukin-6 (IL-6) levels, bacteremia, and sepsis mort
200 expression of the pro-inflammatory cytokine interleukin-6 (IL-6) relative to BALB/cJ and PDE11A WT m
203 er levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6), more neutrophil recruitment, and a
205 tic livers of beta2SP(+/-) mice treated with interleukin-6 (pIL6; (IL6) beta2SP(+/-) LSCs) were highl
206 igher AT1RaAbs correlated significantly with interleukin-6 (Spearman r=0.33, P<0.0001), systolic bloo
209 ated the association between higher maternal interleukin-6 concentrations and lower impulse control.
212 es to map integratively the epitope of human interleukin-6 receptor (IL-6R) for two adnectins with di
214 uated glutamate uptake, intramyelinic edema, interleukin-6 release, complement activation, inflammato
216 ological indicator of maternal inflammation (interleukin-6) that has been shown to influence fetal br
217 e expression of tumor necrosis factor alpha, interleukin-6, and interleukin-8 in the respiratory trac
218 prostaglandin E2, epinephrine, TNFalpha, and interleukin-6, and the neuropathic pain induced by the c
219 al, and cardiometabolic factors, and CRP and interleukin-6, each standard deviation increase in sCD14
220 tive catalase; and 3) selective secretion of interleukin-6, interleukin-10, and vascular endothelial
221 of proinflammatory cytokines (interleukin-3, interleukin-6, interleukin-13, interleukin-17, macrophag
222 al injury (angiopoietin-2) and inflammation (interleukin-6, interleukin-8, and interleukin-33 and sol
225 ducts, surfactant protein D, angiopoietin-2, interleukin-6, interleukin-8, interleukin-33, and solubl
226 er N-acetyl-l-cysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligan
229 ), a linchpin in the pre-B-cell receptor and interleukin 7 receptor signaling pathways critical to B-
231 meostatic proliferation of infected cells by interleukin-7 (IL-7) or antigenic stimulation, as well a
232 ression of multiple hematopoietic cytokines (interleukin-7 [IL-7], Flt3L, stem cell factor [SCF], ThP
233 were associated with increased expression of interleukin 8 (IL-8), CXCL2, IL-1beta, tumor necrosis fa
234 ection were assessed by measuring release of interleukin 8 from AGS cells (to detect cag pathogenicit
236 ered genes include humanin-like-8 (MTRNRL8), interleukin-8 (IL8), and serpin peptidase inhibitor, cla
238 er interleukin-15 concentrations, and higher interleukin-8 concentrations, than were no acute exacerb
240 spholipase A2; at CYP2F1, with higher plasma interleukin-8 concentrations; at TREH, with lower concen
242 or necrosis factor alpha, interleukin-6, and interleukin-8 in the respiratory tract and central nervo
243 opoietin-2) and inflammation (interleukin-6, interleukin-8, and interleukin-33 and soluble suppressio
244 ssion model incorporating oxygenation index, interleukin-8, and tumor necrosis factor-R2 was superior
247 nt protein D, angiopoietin-2, interleukin-6, interleukin-8, interleukin-33, and soluble suppression o
248 ivariable analysis included higher levels of interleukin-8, monocyte chemoattractant protein-1, resis
250 ysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligand 8, and monocy
252 T cells lacking Atg3 or Atg5 have increased interleukin-9 (IL-9) expression upon differentiation int
253 ow that, in mice and humans, a population of interleukin-9 (IL-9)-producing T cells activated via the
254 ts most likely to benefit from targeted anti-interleukin and anti-immunoglobulin E therapies, and in
256 rvastatin was able to block the induction of interleukins IL-6 and IL-8 triggered by pathologic stimu
257 ion of proinflammatory biomarkers, including interleukin (IL) 1beta, tumor necrosis factor alpha (TNF
258 study evaluates whether specific patterns of interleukin (IL)-1 gene variants, known to affect period
259 Increasing evidence has linked dysregulated interleukin (IL)-10 production by IL-10(+ve) B cells to
263 Increased level of proinflammatory cytokine interleukin (IL)-12 correlates with the severity of peri
264 says quantified tumor necrosis factor (TNF), interleukin (IL)-12, and IL-10 in gingival tissues.
269 the effects of lipopolysaccharides (LPS) and interleukin (IL)-17A on the activation of macrophages in
273 treated with anakinra, an antagonist of the interleukin (IL)-1beta receptor (IL-1R), or harboring a
274 ession of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 in the synovial membran
275 ancer risk associated with concentrations of interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, IL-12,
276 molars were collected for quantification of interleukin (IL)-1beta, IL-4, IL-6, IL-17, and tumor nec
277 iants include polymorphisms in the genes for interleukin (IL)-1beta, IL-6, IL-10, monocyte chemoattra
279 gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-2, but not IL-17A; iii) high-affinity M
283 (MSC) numbers, type 2-associated cytokines (interleukin (IL)-33, thymic stromal lymphopoietin, IL-5
284 trated the role of interferon (IFN)gamma and interleukin (IL)-4 in polarizing these cells towards a M
287 This is distinct from the response evoked by interleukin (IL)-6 that is known to induce both pro infl
289 eased interferon-gamma-inducible protein 10, interleukin (IL)-6, IL-8, vascular endothelial growth fa
292 s in mice stimulated secretion of cytokines (interleukin [IL] 25, IL33, and thymic stromal lymphopoie
293 As associated with a type 2 immune response (interleukin [IL]5 gene, IL13, and IL13RA2) and a type 17
294 K-2 induced the expression of CCL4, CCL5 and interleukin(IL)-1beta in HD11 cells and CCL4 and CCL5 in
295 gut homeostasis through the immunomodulatory interleukin IL10, but there is little knowledge on how t
298 al multidomain structure: an N-terminal Toll-interleukin receptor (TIR) or coiled-coil (CC) domain, a
299 common gamma chain, which is part of several interleukin receptors, including IL-2 and IL-7 receptors
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