ライフサイエンスコーパス: interleukin

1 D (controls), we measured soluble markers of interleukin 1 (IL-1) activation at 4 different time poin

2 Interleukin 1 beta (IL1B) increases intestinal permeabil

3 roglial numbers, increased interleukin 6 and interleukin 1 receptor antagonist messenger RNA, alterat

4 with mice lacking signaling through the Toll-Interleukin 1 Receptor Domain-Containing Adaptor Protein

5 terleukin-1beta interacts with its receptor (interleukin 1 receptor type 1) on hematopoietic stem and

6 of monocytes/macrophages, granulocytes, and interleukin 1 signaling was investigated using depletion

7 d Nck1's proinflammatory role by identifying interleukin 1 type I receptor kinase-1 (IRAK-1) as a Nck

8 tricles, inversely associated to CRP and IL (interleukin)-1 changes in acute infection patients.

9 ion often termed a "cytokine storm." Because interleukin-1 (IL-1) blocks the production of IL-6 and o

10 ced proinflammatory cytokines in response to interleukin-1 (IL-1) or tumor necrosis factor alpha (TNF

11 s, Legionella-infected macrophages induce an interleukin-1 (IL-1)-dependent inflammatory cytokine res

12 ow (BM) via a type II interferon (IFN-II) or interleukin-1 (IL1) response, respectively, which confer

13 n of either MYD88, IRAK4, or IRAK1 abolished interleukin-1 beta (IL-1beta) signaling; however, we wer

14 Interleukin-1 has been implicated as a mediator of recur

15 neurodegenerative process(5-8), and its Toll/interleukin-1 receptor (TIR) domain exerts its pro-neuro

16 88 L265P mutant results in the activation of interleukin-1 receptor associated kinase (IRAK).

17 Sterile alpha and Toll/interleukin-1 receptor motif-containing protein 1 (SARM1

18 TGFbeta1 (transforming growth factor beta1), interleukin-1, TNF-alpha, and BDNF signaling pathways.

19 bant (bradykinin-B2-antagonist) or anakinra (interleukin-1-antagonist) reduces disease activity in pa

20 Interleukin 10 (IL-10) is an anti-inflammatory cytokine

21 interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 22 (IL-22), and tumo

22 cal source of the anti-inflammatory cytokine interleukin-10 (IL-10) and the metalloproteinase MMP9.

23 Here, we explored the role of the interleukin-10 (IL-10) axis in restoring murine microgli

24 bitory signals, including increased PD-1 and interleukin-10 (IL-10) expression by cytotoxic T cells i

25 Interleukin-10 (IL-10) is a dimeric cytokine with both i

26 We have previously shown that expression of Interleukin-10 (IL-10), a classical anti-inflammatory cy

27 ry human tissues, activate anti-inflammatory interleukin-10 and improve colitis symptoms in a colitis

28 the anti-inflammatory markers arginase 1 and interleukin-10 in murine BMDMs.

29 erleukin-6, tumor necrosis factor-alpha, and interleukin-10 levels in vivo.

30 ctive: To determine the mechanisms of IL-10 (interleukin-10) deficient-EPC-derived exosome dysfunctio

31 retion of protective immunomodulatory factor interleukin-10.

32 ed to an immunostimulatory cytokine, such as interleukin 12 (IL-12) (rNDV-anti-CD28-murine IL-12 [mIL

33 toxic T cells and natural killer cells), and interleukin 12 production by antigen-presenting cells co

34 Interleukin-12 (IL-12) is a powerful cytokine that activ

35 donor T cells while releasing cytokines (eg, interleukin-12 [IL-12], IL-23, IL-6, IL-27, IL-10, trans

36 tcome of anti-tumor necrosis factor and anti-interleukin-12/interleukin-23 treatment on SB and coloni

37 -type infection, instead promoting sustained interleukin 12p40 (IL-12p40) induction and increased IL-

38 date intrathecal delivery of EPHA2, HER2 and interleukin 13 receptor alpha2 chimeric antigen receptor

39 report a role for the type 2 cytokine interleukin-13 in orchestrating metabolic reprogramming

40 Interleukin 15 (IL-15) is an essential cytokine for the

41 oing CD8alpha depletion and treated with the interleukin-15 (IL-15) superagonist N-803 (J.

42 pecific chimeric antigen receptor (CAR) with interleukin-15 in children with relapsed or resistant ne

43 In a subset of 71 participants, interleukin-15 levels (median fluorescent intensity) wer

44 expressing genes that encode anti-CD19 CAR, interleukin-15, and inducible caspase 9 as a safety swit

45 ns convincingly show that T-helper 17 (Th17)/interleukin 17 (IL-17)-driven immunity is essential to c

46 production of two proinflammatory cytokines: interleukin-17 (IL-17) and GM-CSF.

47 olleagues demonstrate that the production of interleukin-17 (IL-17) during inflammation promotes soci

48 pro-inflammatory roles, the ancient cytokine interleukin-17 (IL-17) modulates neural circuit function

49 wnstream signaling JAK pathway genes and the interleukin-17 (IL-17) pathway.

50 describe that interleukin-17 (IL-17) re-programs the urea cycle in ker

51 Interleukin-17 and epidermal growth factor were identifi

52 inflammatory and chemotactic cytokines, less interleukin-17 production, and reduced fibrosis formatio

53 Interleukin-17 receptor D (IL-17RD), also known as simil

54 Dual neutralisation of interleukin 17A (IL17A) and interleukin 17F (IL17F) is a

55 nes (IL-1alpha [interleukin 1alpha], IL-17A [interleukin 17A], P<0.05) in comparison with controls.

56 FSTL-1 Hypo mice had increased Il17a/interleukin-17A (IL-17A) and IL-17-dependent cytokine ex

57 levels of proinflammatory cytokines, such as interleukin-17A (IL-17A) and IL-1alpha, compared to thos

58 Interleukin-17A (IL-17A) is a pro-inflammatory cytokine

59 eutralisation of interleukin 17A (IL17A) and interleukin 17F (IL17F) is a potential novel therapeutic

60 t the deubiquitinase Cyld prevents excessive interleukin 18 (IL-18) production in the colonic mucosa

61 , ATX, and Mac2BP levels declined by week 2, interleukin 18 levels declined by the end of treatment,

62 oluble CD163 (sCD163), interleukin 6 (IL-6), interleukin 18, monocyte chemoattractant protein (MCP-1)

63 munotherapy, we found that components of the interleukin-18 (IL-18) pathway are upregulated on tumour

64 stically, Tak1 activation leads to increased interleukin-18 (IL-18) production, whereas blockade of I

65 inflammasome as the major pathway leading to interleukin-18 (IL-18) release and restriction of S Typh

66 (>0.3 x 10(9) /L) at screening and low serum interleukin-18 relative change at pre-treatment baseline

67 nts with high blood eosinophils or low serum interleukin-18 response are potential subgroups for furt

68 min-D-dependent pyroptosis and processing of interleukin-18, thereby destroying the replicative niche

69 uent release of mature interleukin-1beta and interleukin-18.

70 d by serum interferon-induced protein 10 and interleukin 1alpha, is independently associated with inc

71 nd plasma inflammatory cytokines (IL-1alpha [interleukin 1alpha], IL-17A [interleukin 17A], P<0.05) i

72 derived cytokines tumour necrosis factor and interleukin-1alpha stimulated reactive oxygen species an

73 ototypic inflammatory IL (interleukin) IL1B (interleukin 1B), IL6, IL8, the inflammasome NLRP3, and t

74 s of proinflammatory macrophages showing IL (interleukin) 1B or TNF (tumor necrosis factor) expressio

75 Interleukin-1b and interferon-gamma levels were upregula

76 and secretion of inflammatory cytokines (IL [interleukin] 1B, IL6, and TNF [tumor necrosis factor]).

77 which leads to the proteolytic maturation of interleukin 1beta (IL-1beta) and pyroptosis.

78 RP3 inflammasome and consequent secretion of interleukin 1beta (IL-1beta).

79 pase-1 (CASP1) cleavage, and proinflammatory interleukin 1beta (IL1B) maturation.

80 a2) and inflammation (tumor necrosis factor, interleukin 1beta).

81 ne marrow-derived macrophages by suppressing interleukin 1beta, CD68, and phagocytosis but not CD208,

82 resistant to reactivation by vorinostat and interleukin 1beta.

83 ased secretion of inflammatory cytokines IL (interleukin)-1beta (98%, P<0.0001) and IL-6 (460%, P<0.0

84 Whether inhibition of interleukin-1beta (IL-1beta) can reduce the consequences

85 The alarm cytokine interleukin-1beta (IL-1beta) is a potent activator of th

86 LPA also induced expression of interleukin-1beta (IL-1beta) mRNA but no significant inc

87 as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) a

88 e phase of MIS-C, we observed high levels of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-17,

89 ion and release of the inflammatory cytokine interleukin-1beta (IL-1beta).

90 that RBP4 primes the NLRP3 inflammasome for interleukin-1beta (IL1beta) release, in a glucose-depend

91 spase-1 and the subsequent release of mature interleukin-1beta and interleukin-18.

92 Over time, a decrease in osteoprotegerin and interleukin-1beta concentrations in PICF along with an i

93 lso reduced neuro-inflammation by decreasing interleukin-1beta expression, activation of astrocytes,

94 The released interleukin-1beta interacts with its receptor (interleuk

95 female mice, as well as increased VEGFR1 and interleukin-1beta mRNA expression in females, and reduce

96 This metabolite potentiates interleukin-1beta production, resulting in hyperinflamma

97 nflammasome in naive neutrophils and promote interleukin-1beta secretion.

98 mily pyrin domain-containing 3 inflammasome, interleukin-1beta) in neutrophils suppress granulopoiesi

99 terleukin-6, tumor necrosis factor-alpha and interleukin-1beta), rebalanced levels of short-chain fat

100 lerated with upregulated type I collagen and interleukin-1beta, and downregulated matrix metalloprote

101 enchymal stromal cells reduced astrogliosis, interleukin-1beta, and monocyte chemoattractant protein-

102 kers, including tumor necrosis factor-alpha, interleukin-1beta, and nitric oxide synthase-2, highligh

103 urvival rate, but reduced levels of systemic interleukin-1beta, interleukin-6, and monocyte chemoattr

104 rrier dysfunction, astrocyte activation, and interleukin-1beta, interleukin-6, tumor necrosis factor-

105 ytes from TBI + Sp mice had higher levels of interleukin-1beta, tumor necrosis factor-alpha, and reac

106 y genes, including tumor necrosis factor and interleukin-1beta.

107 l cytokines over a 24-hour period, including interleukin-1RA, interleukin-6, interleukin-8, G-CSF, an

108 epletion of IFN-gamma or genetic deletion of interleukin 2 (IL-2) receptor common gamma chain in Rag-

109 flammatory cytokines in the serum, including interleukin 2 (IL-2), IL-6, IL-12 (p70), tumor necrosis

110 on of CD8alpha but not PD1, TIM-3, CTLA4, or interleukin 2 (IL-2).

111 peutic regimen of low-dose recombinant human interleukin-2 (IL-2) combined with low-dose rapamycin to

112 Interleukin-2 (IL-2) is a component of most protocols of

113 Interleukin-2 (IL-2) is a small alpha-helical cytokine t

114 filtrating CD4(+), and this was prevented by interleukin-2 (IL-2) neutralization.

115 Low-dose interleukin-2 (IL-2) represents a new therapeutic approa

116 ), donor T(regs) failed to engraft even with interleukin-2 (IL-2) support.

117 d the sensitivity of T cells to the cytokine interleukin-2 (IL-2) through a positive feed-forward loo

118 -fold (CI, 3.5- to 18.0-fold; P < 0.001) for interleukin-2 (IL-2), and 1.7-fold (CI, 0.1- to 4.0-fold

119 zed Nfkappab1 mRNAs and reduced secretion of interleukin-2 (IL2) and interferon-gamma (IFNgamma), two

120 Interleukin-2 appeared to be the earliest, most sensitiv

121 Symptoms and plasma interleukin-2 levels increased significantly or near sig

122 nd CD4+ T-cell (expressing interferon-gamma, interleukin-2, and CD40 ligand) responses were evaluated

123 Interleukin 22 (IL-22) signals via both IL-22 receptor a

124 nterleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 22 (IL-22), and tumor necrosis factor alpha

125 onstrate that mice lacking IL-17RA, Act1, or interleukin 22 showed no evidence for altered VVC suscep

126 The cytokine interleukin-22 (IL-22) is a critical regulator of epithe

127 these profiles, with a nearly total loss of interleukin-22 (IL-22) production in the tonsil and colo

128 Our studies revealed that the interleukin-22 (IL-22)/IL-17-producing ILCS was not alte

129 re associated with SNPs in the IL-23R or the interleukin-23 (IL-23) cytokine itself and related downs

130 Guselkumab, a specific inhibitor of interleukin-23 (IL-23) via IL-23 p19 subunit binding, si

131 The interleukin-23 (IL-23)/T-helper 17 cell pathway is impli

132 d high affinity and selectivity to the human interleukin-23 (IL-23R) and IL-17 receptor A were used.

133 umor necrosis factor and anti-interleukin-12/interleukin-23 treatment on SB and colonic ACE2 expressi

134 ILC2 activation requires tuft-cell-derived interleukin-25 (IL-25), but whether additional signals r

135 blished that the immune-suppressive cytokine interleukin-27 (IL-27) is elevated in neonatal mice.

136 alpha (TNFalpha)-mediated pathway regulating interleukin-27 receptor subunit alpha (IL-27Ra) expressi

137 We found high amounts of interleukin 31 (IL-31) in skin wound tissue during the p

138 Interleukin-33 (IL-33) acts as an alarmin cytokine by al

139 We find that the cytokine interleukin-33 (IL-33) is expressed by adult hippocampal

140 cilitates the release of a nuclear cytokine, interleukin-33 (IL-33).

141 -1R), which has two known ligands: CSF-1 and interleukin-34 (IL-34).

142 Dupilumab, an anti-IL (Interleukin) -4 receptoralpha mAb, inhibits IL-4/IL-13 s

143 Interleukin-4 (IL-4) is crucial in many helminth infecti

144 by tumor-associated microglia in response to interleukin-4 (IL-4) stimulation.

145 Interleukin-4 (IL-4) suppresses the development of multi

146 onse is dependent on the T helper 2 cytokine interleukin-4 (IL-4), but not the T helper 1 cytokine in

147 n airway type 2 cytokine activity, including interleukin-4 (IL-4), IL-5, and IL-13, are now establish

148 growth factor beta 1 (TGF-beta1) because of interleukin-4 (IL-4)- and signal transducer and activato

149 h, a process dependent on the T(H)2 cytokine interleukin-4 (IL-4).

150 The anti-inflammatory cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 we

151 gic testing showed exaggerated production of interleukin-4 and reduced production of interferon-gamma

152 is directly involved in fusogenic cytokine (interleukin-4 plus granulocyte macrophage-colony stimula

153 inical improvement of AD that is mediated by interleukin-4 receptor alpha inhibition and the subseque

154 Dupilumab is a fully human antibody to interleukin-4 receptor alpha that improves the signs and

155 Finally, we showed that interleukin-4 treatment was sufficient to increase the n

156 ncept, we developed a 5-plex assay measuring interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin

157 T-helper type 1 (Th1) cells but increases in interleukin 5-expressing Th2 cells and eosinophils in pe

158 type 2 (anti-helminths) effectors, including interleukin-5 (IL-5), IL-13, immunoglobulin E and eosino

159 IgE in serum, and increased eosinophilia and interleukin-5 in bronchoalveolar lavage (BAL) compared t

160 Circulating interleukin 6 (IL-6) levels surge during exercise and IL

161 rved that GM-CSF was not regulated by either interleukin 6 (IL-6) or IL-23, which are both potent ind

162 We used hyperalgesic priming with interleukin 6 (IL-6) priming and PGE(2) as a second stim

163 flammatory markers C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (T

164 ion of early inflammatory markers, including interleukin 6 (IL-6), IL-1alpha, and tumor necrosis fact

165 and in vivo, including the up-regulation of interleukin 6 (IL-6), IL-23, Arginase1, as well as surfa

166 5-plex assay measuring interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin 10 (IL-10), interleuki

167 nducible protein 10, soluble CD163 (sCD163), interleukin 6 (IL-6), interleukin 18, monocyte chemoattr

168 articles was introduced for the detection of interleukin 6 (IL-6).

169 It is established that interleukin 6 (IL6) regulates multiple aspects of metabo

170 h as augmented microglial numbers, increased interleukin 6 and interleukin 1 receptor antagonist mess

171 LOY was modestly inversely associated with interleukin 6 in postmenopausal women (P = 0.03).

172 r of tumor necrosis factor alpha (TNFalpha), interleukin 6 receptor (IL-6R), and epidermal growth fac

173 ic inflammation (soluble CD163 and CD14, and interleukin 6) and levels of T-cell immune activation (H

174 protein 1, tumor necrosis factor alpha, and interleukin 6) through YAP association with the TEA doma

175 n in the expression levels of p21, mTOR/pS6, interleukin 6, and tumor necrosis factor alpha in skin a

176 ice and found that aging led to elevated IL (interleukin)-6 levels and mitochondrial dysfunction, ass

177 Interleukin-6 (-24.9 pg/mL vs 442.8 pg/mL; P = .032) con

178 NF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) after chelation therapy.

179 ncreased levels of the inflammatory cytokine interleukin-6 (IL-6) and decreased levels of IL-12, IFN-

180 ld application, we establish that endogenous interleukin-6 (IL-6) can be quantified in 2-uL serum sam

181 Interleukin-6 (IL-6) has emerged as a key component of t

182 Interleukin-6 (IL-6) induced hepcidin expression is a ke

183 Interleukin-6 (IL-6) is a cytokine with critical innate

184 Interleukin-6 (IL-6) is a pleiotropic cytokine that has

185 The interleukin-6 (IL-6) membrane receptor and its circulati

186 tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) mRNAs, as well as IFN-alpha, IFN-be

187 nflammatory effects, including inhibition of interleukin-6 (IL-6) that plays a key role in the develo

188 lating microglia are critically dependent on interleukin-6 (IL-6) trans-signaling via the soluble IL-

189 ation analyses suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are l

190 s had less severe illness); and (3) elevated interleukin-6 (IL-6), IL-8, and myeloperoxidase levels i

191 in response to the proinflammatory cytokine interleukin-6 (IL-6), suggesting that MSH3 may be a shut

192 matory markers, C-reactive protein (CRP) and interleukin-6 (IL-6).

193 slet-derived protein 3alpha (REG3alpha), and interleukin-6 (IL-6).

194 The cytokine interleukin-6 (IL6) and its downstream effector STAT3 co

195 Furthermore, interleukin-6 (IL6), IL17, IGFBP4, and MMP13 were signif

196 ritin (odds ratio [OR], 2.40; P < 0.001) and interleukin-6 (OR, 1.45; P = 0.009).

197 an also directly activate KSHV-encoded viral interleukin-6 (vIL-6) and, thus, contribute to the patho

198 Human herpesvirus 8 (HHV-8) viral interleukin-6 (vIL-6) is a cytokine that is poorly secre

199 KSHV viral interleukin-6 (vIL-6) is a viral homolog of human IL-6 (

200 CE Human herpesvirus 8 (HHV-8)-encoded viral interleukin-6 (vIL-6) was the first viral IL-6 homologue

201 ytic replication and directly activate viral interleukin-6 (vIL-6).

202 cium binding adaptor molecule-1 [Iba-1]) and interleukin-6 [IL-6]) and astrogliosis/astrocyte damage

203 Interleukin-6 and -10, tumor necrosis factor-alpha, and

204 ion of colchicine attenuated the increase in interleukin-6 and high-sensitivity C-reactive protein co

205 forming growth factor beta (TGFbeta) and LIF interleukin-6 family cytokine (LIF) signaling pathways.

206 80) outperformed clinical markers and plasma interleukin-6 for prospectively predicting trauma patien

207 r factor-kB, tumor necrosis factor-alpha and interleukin-6 gene expression in prefrontal cortex.

208 ising therapies, including antiviral agents, interleukin-6 inhibitors, and convalescent serum.

209 alysis, the association of sodium levels and interleukin-6 levels (which has been linked to nonosmoti

210 Higher interleukin-6 levels correlated with lower sodium levels

211 um lactate dehydrogenase, procalcitonin, and interleukin-6 levels.

212 n markers were suggestive of cytokine storm (interleukin-6 median, 135 pg/mL) and macrophage activati

213 144 (77%), glucocorticoids in 91 (49%), and interleukin-6 or 1RA inhibitors in 38 (20%).

214 lations, the safety and efficacy of the anti-interleukin-6 receptor antibody tocilizumab in patients

215 The efficacy of interleukin-6 receptor blockade in hospitalized patients

216 humanised monoclonal antibody targeting the interleukin-6 receptor, reduced the risk of relapse in p

217 serum monocyte chemoattractant protein-1 and interleukin-6 were significantly increased.

218 to 3) associations between circulating IL6 (interleukin-6) and NT-proBNP (N terminal pro B-type natr

219 luble tumor necrosis factor-receptor I], and interleukin-6), YKL-40 (related to liver injury and infl

220 At hospital discharge, interleukin-6, -8, and -10 retained the association but

221 psis diagnosis and study intervention group, interleukin-6, -8, and -10, tumor necrosis factor-alpha,

222 e up-regulating tumor necrosis factor alpha, interleukin-6, and C-X-C motif chemokine ligand 1 expres

223 adhesion molecule, thrombomodulin, endocan, interleukin-6, and interleukin-8 than those without acut

224 inflammatory biomarkers (C-reactive protein, interleukin-6, and interleukin-8) were measured from per

225 educed levels of systemic interleukin-1beta, interleukin-6, and monocyte chemoattractant protein-1.

226 ceptor expressed on myeloid cells [sTREM-1], interleukin-6, interleukin-8, chitinase-3-like protein-1

227 a 24-hour period, including interleukin-1RA, interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.00

228 ion of pro-inflammatory cytokines (including interleukin-6, tumor necrosis factor-alpha and interleuk

229 astrocyte activation, and interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and interleu

230 ed that in addition to type-I interferon and interleukin-6-dependent inflammatory responses, infectio

231 Anti-interleukin-6-directed therapies are highly effective in

232 Mutational patterns confirm that the interleukin-6-JAK1-STAT3 pathway is deregulated.

233 a significant association between cord serum interleukin-7 at birth and the trajectories of children'

234 quiescent CD4 T cells (cultured with 2 ng/ml interleukin-7).

235 activated B cells (NF-kappaB) activation and interleukin-8 (IL-8) secretion are attributed to T4SS-de

236 trial of cerebral palsy, the level of plasma interleukin-8 (IL-8) was increased, correlated with moto

237 uction of several cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic ce

238 y response characterized by the secretion of interleukin-8 (IL-8; also called CXCL8) and the expressi

239 Although elevated plasma interleukin-8 (pIL-8) has been associated with poor outc

240 Interleukin-8 and S-100beta levels in quartile 4 were al

241 d hyperproteinorrachia, and showed increased interleukin-8 and tumor necrosis factor-alpha concentrat

242 There was no difference in interleukin-8 levels.

243 hagocytosis promotes killing of S aureus and interleukin-8 release by neutrophils.

244 nce, biofilm formation, and pro-inflammatory interleukin-8 secretion compared with ST31 isolates.

245 thrombomodulin, endocan, interleukin-6, and interleukin-8 than those without acute respiratory distr

246 kers (C-reactive protein, interleukin-6, and interleukin-8) were measured from peripheral plasma coll

247 d on myeloid cells [sTREM-1], interleukin-6, interleukin-8, chitinase-3-like protein-1, soluble tumor

248 d, including interleukin-1RA, interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.001).

249 st that hypothesis, we intranasally infected interleukin-8R2 (IL-8R2) (Cxcr2)-deficient mice on a BAL

250 x gene promoters and active H3K4me3 marks on interleukin, defensin, and chemokine gene promoters, fac

251 tigen (PCNA), the anti-inflammatory cytokine interleukin (IL) 10, and the apoptosis markers caspase 3

252 Interleukin (IL) 11 activates multiple intracellular sig

253 with low serum albumin and iron], and serum interleukin (IL) 1beta were positively associated with D

254 Using a multiplex immunoassay, we measured interleukin (IL) 1beta, IL-6, tumor necrosis factor alph

255 We investigate the effects of interleukin (IL) 22 in the development of pancreatic tum

256 numbers of intracellular 11G5, secretion of interleukin (IL) 6 and IL8, and markers of DNA double-st

257 of the Toll-like receptor (TLR)-related lnc interleukin (IL) 7 receptor (IL7R) were significantly re

258 MeONPs to screen a proinflammatory cytokine interleukin (IL)-1 beta (IL-1beta) release in THP-1 cell

259 r tyrosine kinase AXL, while upregulation of interleukin (IL)-12 depends strictly on interferon-gamma

260 Interleukin (IL)-13 is a type 2 cytokine with important

261 ern that included interferon (IFN)-gamma and interleukin (IL)-13.

262 that stimulate T cell proliferation, such as interleukin (IL)-15, have been explored as a means of bo

263 clerosing cholangitis (PSC) show a prominent interleukin (IL)-17 response upon stimulation with bacte

264 Interleukin (IL)-17a has been highly conserved during ev

265 ndependently associated with lower levels of interleukin (IL)-18 and IL-6 before and up to 12 weeks p

266 B cell production of interleukin (IL)-1beta and IL-6 is markedly upregulated

267 Inflammation reduction with the interleukin (IL)-1beta inhibitor canakinumab significant

268 Inhibition of the interleukin (IL)-1beta innate immunity pathway is associ

269 The cytokine interleukin (IL)-1beta is a key mediator of antimicrobia

270 Interleukin (IL)-1beta is a main inducer of inflammation

271 Interleukin (IL)-1beta microinjected in the nucleus trac

272 migration-induced cell shattering, releasing interleukin (IL)-1beta that drives granulocyte-macrophag

273 Inflammatory cytokines, such as interleukin (IL)-1beta, alter iron homeostasis and eryth

274 Colonic interleukin (IL)-1beta, IL-6, and malondialdehyde (MDA)

275 Cleavage of pro-interleukin (IL)-1beta, pro-IL-18, and gasdermin-D by ac

276 sis of extracellular ATP (eATP) could affect interleukin (IL)-1beta-induced CXCL8 secretion.

277 Interleukin (IL)-2 and IL-21 dichotomously shape CD8(+)

278 Treatment with interleukin (IL)-22, a cytokine with multiple targets, a

279 Here, we show that interleukin (IL)-22, induced by colonization of the gut

280 phoid cells (ILC3) that continuously produce interleukin (IL)-22.

281 ulation of these cells depends critically on interleukin (IL)-33 produced by local mesenchymal stroma

282 ) regulatory T (T(reg)) cells expressing the interleukin (IL)-33 receptor ST2 mediate tissue repair i

283 across the plasma membrane of HBE cells and interleukin (IL)-33 release into the extracellular media

284 Interleukin (IL)-4 and IL-13 are both pivotal cytokines

285 d migration, release of the type 2 cytokines interleukin (IL)-4, IL-5 and IL-13 from T helper 2 (Th2)

286 in the periphery and liver, increased serum interleukin (IL)-6 and IL-2, but peripheral regulatory T

287 ing factor, tumor necrosis factor alpha, and interleukin (IL)-6 secretion.

288 gy and excessive production of the cytokines interleukin (IL)-6, IL-10, transforming growth factor be

289 Increased plasma levels of soluble CD25, interleukin (IL)-6, IL-1beta, tumor necrosis factor-alph

290 id multiplex cytokine assay to measure serum interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-al

291 primary response 88, interferon (IFN)-gamma, interleukin (IL)1-beta, tumor necrosis factor alpha, cas

292 ction of l-arginine in mice with deletion of interleukin (IL)12B, NLRP3, or IL18 and in mice given MC

293 Interleukin (IL)33/IL1F11 is an important mediator for t

294 overlapped with those associated with death (interleukin [IL]-1beta, IL-6).

295 <0.05) increase in the inflammatory markers (interleukin [IL]-1beta, IL-6, and tumor necrosis factor-

296 ss [OSI], tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, matrix metalloproteinase [MMP]-8

297 chemokine [C-X-C motif] ligand 1 [CXCL1] and interleukin [IL]-8).

298 Gamma chain (gammac) cytokines (interleukin [IL]2, IL4, IL7, IL9, IL15, and IL21) signal

299 ologically is driven by the type 2 cytokines Interleukin-(IL)-4, IL-5, and IL-13.

300 d genes were the prototypic inflammatory IL (interleukin) IL1B (interleukin 1B), IL6, IL8, the inflam