ライフサイエンスコーパス: IL-18

1 IL-18 activity is modulated in vivo by its naturally occ

2 IL-18 and its receptor are members of these families.

3 IL-18 binding protein (IL-18BP) acts as a naturally occu

4 IL-18 is a member of the IL-1 family involved in innate

5 IL-18 is a proinflammatory cytokine made upon activation

6 IL-18 is produced as inactive proform and has to be clea

7 IL-18 is recognized as binding to the protein products o

8 IL-18 levels were measured in 14 additional chronically

9 IL-18 levels were significantly higher in HIV monoinfect

10 IL-18 plays an important role in host innate and adaptiv

11 IL-18 was significantly elevated in coinfected individua

12 g elevations in heat-shock protein 70, IL-1, IL-18, and TNFalpha indicative of a sterile inflammatory

13 ociated lipocalin, kidney injury molecule-1, IL-18, and liver-type fatty acid binding protein with gr

14 ntly respond to skin commensals in an IL-1-, IL-18-, and antigen-dependent manner.

15 atitis induced by either cerulein or IL-12 + IL-18.

16 lation with E. coli or interleukin (lL)-12 + IL-18 as compared with circulating MAIT cells.

17 sing these tools, we demonstrate that IL-12, IL-18, and TLRs are completely dispensable for the TCR a

18 tablished, the exact contributions of IL-12, IL-18, and TLRs remain unclear for these two activation

19 ol (p = 0.006) decreases interleukin (IL)-12/IL-18-induced interferon-gamma (IFN-gamma) production ve

20 IFN-gamma following administration of IL-12/IL-18 versus control-fed animals (p < 0.0001).

21 indicate genistein and equol decrease IL-12/IL-18-induced IFN-gamma production by human NK cell subs

22 vation of C5aR2 in NK cells suppressed IL-12/IL-18-induced IFN-gamma production.

23 gnal transduction, genistein decreases IL-12/IL-18-induced total phosphorylated tyrosine, and phospho

24 Further, genistein limits IL-12/IL-18-mediated upregulation of IL-18Ralpha expression on

25 -10, HGF, IL-6, MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and IL-1RA significantly correlat

26 nase Cyld prevents excessive interleukin 18 (IL-18) production in the colonic mucosa by deubiquitinat

27 red B cell activation during interleukin 18 (IL-18)-induced chronic inflammation.

28 Extreme elevation of serum interleukin-18 (IL-18) has been observed specifically in patients with M

29 Interleukin-18 (IL-18) is a pleiotropic pro-inflammatory cytokine belong

30 found that components of the interleukin-18 (IL-18) pathway are upregulated on tumour-infiltrating ly

31 ctivation leads to increased interleukin-18 (IL-18) production, whereas blockade of IL-18 receptor in

32 the major pathway leading to interleukin-18 (IL-18) release and restriction of S Typhimurium replicat

33 Endothelial cell-derived interleukin-18 (IL-18) selectively expands a T-cell population (CD4+CD45

34 473) can induce secretion of interleukin-18 (IL-18) through activation of the inflammasome in both my

35 idney injury markers such as interleukin-18 (IL-18), connective tissue growth factor (CTGF), neutroph

36 nterleukin-1beta (IL-1beta), interleukin-18 (IL-18), nucleotide-binding domain, leucine rich family (

37 uced levels of interleukin 1beta (IL-1beta), IL-18, and gamma interferon (IFN-gamma) in sera.

38 ependent on T-bet and regulated by IL-1beta, IL-18 and Notch signals.

39 f EVs, resulting in alterations in IL-1beta, IL-18, and caspase-1 activity.

40 om KI mice secreted high levels of IL-1beta, IL-18, and IL-1alpha but low amounts of IL-1 receptor an

41 mechanisms underpinning IL-1alpha, IL-1beta, IL-18, and IL-37 maturation and release; and the functio

42 IL-1beta, IL-18, and IL-37 maturation and secretion is governed by

43 pase-1 and gasdermin D; release of IL-1beta, IL-18, caspase-1, and lactate dehydrogenase from the cel

44 responses including production of IL-1beta, IL-18, eicosanoids and pyroptotic cell death.

45 mmatory family members (IL-1alpha, IL-1beta, IL-18, IL-33, IL-36alpha, IL-36beta and IL-36gamma) are

46 with agonist activity (IL-1alpha, IL-1beta, IL-18, IL-33, IL-36alpha, IL-36beta, and IL-36gamma), re

47 dominated microenvironment (eotaxin-2, IL-5, IL-18, and IL-13) and increased signalling molecules tha

48 rs of macrophage activation: IL-1beta, IL-6, IL-18, and chitotriosidase enzyme activity.

49 except for pro-inflammatory cytokines IL-6, IL-18, and MIG, as well as anti-inflammatory IL-2 that w

50 ge colony stimulating factor (GM-CSF), IL-8, IL-18, monocyte chemotactic protein-1 (CCL2) (MCP-1), ti

51 n mice resulted in elevated levels of active IL-18 and severe colonic inflammation following Citrobac

52 erative colitis, the concentration of active IL-18 was inversely correlated with CYLD expression.

53 was not sufficient to neutralize the active IL-18 in irradiated mice, resulting in a radiation dose-

54 Additionally, IL-18 is produced in the brain in medial habenula neuron

55 Here we show that IL-18BP, a high-affinity IL-18 decoy receptor, is frequently upregulated in diver

56 nflammation and support the rationale for an IL-18-driven subclass of hyperinflammation.

57 These data provide evidence of an IL-18-driven NK cell proliferation and priming for skin-

58 naling downstream of the IL-18R, suggests an IL-18-dependent mechanism in driving the proliferative N

59 ase potent immune cytokines such as IL-1 and IL-18, contribute to various diseases.

60 me pathways, NLRP3, ASC, caspase 1, IL-1 and IL-18.

61 vates the proinflammatory cytokines IL-1 and IL-18.

62 e most sensitive markers; elevated IL-10 and IL-18 are additional indicators for ALPS.

63 ted cell sorting; interleukin 10 (IL-10) and IL-18 and soluble FAS ligand (sFASL) were measured by en

64 s mediated by the innate cytokines IL-12 and IL-18 more than MR1-induced TCR signaling, suggesting TC

65 ithout affecting the expression of IL-12 and IL-18 receptors.

66 nd enhanced capacity to respond to IL-12 and IL-18 stimulation.

67 -gamma by NK cells stimulated with IL-12 and IL-18, which is a crucial system for early IFN-gamma pro

68 independent, innate-like recall by IL-12 and IL-18.

69 f pre-mNK cells to be dependent on IL-12 and IL-18.

70 late the Th-1-polarizing cytokines IL-12 and IL-18.

71 ner but are largely contributed by IL-12 and IL-18; v) as MAIT cells are primed by SAgs, they also be

72 ollowing combined interleukin-12 (IL-12) and IL-18 stimulation.

73 had increased secretion of IL-10, IL-12, and IL-18 upon stimulation of peripheral blood mononuclear c

74 onse to superantigens and a later IL-12- and IL-18-dependent, IFNgamma-dominated response to both bac

75 ible-protein 10, interleukin (IL)-12p40, and IL-18 levels decreased early after start of therapy.

76 that upon activation with IL-12, IL-15, and IL-18 human NK cells express NKG2D ligands of the UL16 b

77 cocorticoids together with IL-12, IL-15, and IL-18 not only upregulate PDCD1 transcription, but also

78 tion with interleukin-12 (IL-12), IL-15, and IL-18, exhibit potent antitumor responses, and safely in

79 ng 11 members, among which are IL-1alpha and IL-18.

80 ession of interleukin 1alpha (IL-1alpha) and IL-18.

81 e of the proinflammatory cytokines IL-1B and IL-18 and pyroptotic cell death.

82 e of pro-inflammatory cytokines IL-1beta and IL-18 accompanied by cell death.

83 -inflammatory cytokines such as IL-1beta and IL-18 and a pore-forming protein, gasdermin D, which tri

84 etion of inflammatory cytokines IL-1beta and IL-18 and an inflammatory cell death called pyroptosis.

85 as measured by the secretion of IL-1beta and IL-18 and by pyroptotic cell death, during both stable i

86 inflammatory cytokines such as IL-1beta and IL-18 and concurrent late CAR T cell expansion character

87 the secretion of interleukin (IL)-1beta and IL-18 and drives cell fate towards pyroptosis-a form of

88 ted processing and secretion of IL-1beta and IL-18 and induces the inflammatory cell death, pyroptosi

89 release of the mature cytokines IL-1beta and IL-18 and induction of pyroptosis.

90 f the proinflammatory cytokines IL-1beta and IL-18 and promoting pyroptosis.

91 mmatory cytokines interleukin (IL)-1beta and IL-18 and pyroptosis.

92 In vitro, secretion of both IL-1beta and IL-18 by macrophages or dendritic cells infected with B.

93 ermin D-mediated cell death and IL-1beta and IL-18 cytokine release.

94 and eliciting the production of IL-1beta and IL-18 in addition to inducing a type of inflammatory cel

95 flammasome-associated cytokines IL-1beta and IL-18 in leishmaniasis.

96 ulating levels of interleukin (IL)-1beta and IL-18 in lipopolysaccharide (LPS)-challenged wild-type m

97 tion mediated release of mature IL-1beta and IL-18 in response to canonical stimuli initiated by NOD-

98 sp1(Null) cells did not release IL-1beta and IL-18 in response to NLRC4 activators Salmonella Typhimu

99 n caspase-1 activity as well as IL-1beta and IL-18 levels.

100 the inflammasome, resulting in IL-1beta and IL-18 maturation.

101 leading to an up-regulation of IL-1beta and IL-18 production in human mesothelial cells.

102 rease in hyperlipidemia-induced IL-1beta and IL-18 production, lowered T-helper type-1 immune respons

103 nicalagin, which inhibited both IL-1beta and IL-18 release.

104 crotic liver induced eosinophil IL-1beta and IL-18 secretion, degranulation, and cell death.

105 NLRP3 inflammasome, leading to IL-1beta and IL-18 secretion.

106 Thus, AmB induced IL-1beta and IL-18 secretions, which are reduced by specific inhibito

107 We discovered that IL-1beta and IL-18 share a common secretory pathway that depends upon

108 well as its downstream targets IL-1beta and IL-18 were confined to aggressive prostate cancer cells.

109 and their downstream products (IL-1beta and IL-18) in different brain regions, and promotes activati

110 the pro-inflammatory cytokines IL-1beta and IL-18, alarmins and endogenous danger-associated molecul

111 on of proinflammatory cytokines IL-1beta and IL-18, and increased sensitivity to peritonitis.

112 ng, and facilitate secretion of IL-1beta and IL-18, as well as other signaling pathways.

113 the pro-inflammatory cytokines IL-1beta and IL-18, as well as to gasdermin D-mediated pyroptotic cel

114 flammatory cytokines, including IL-1beta and IL-18, by inducing the oligomerization of the multiprote

115 on, including cytokines such as IL-1beta and IL-18, growth factors such as fibroblast growth factor 2

116 with marked reductions in serum IL-1beta and IL-18, reduced myeloid inflammatory infiltrate in the sk

117 masome led to the production of IL-1beta and IL-18, which activated IL-8 transcription and hepatic NK

118 and secretion of interleukin (IL)-1beta and IL-18, which trigger inflammatory responses to clear inf

119 on of proinflammatory cytokines IL-1beta and IL-18.

120 on of proinflammatory cytokines IL-1beta and IL-18.

121 f the proinflammatory cytokines IL-1beta and IL-18.

122 f the proinflammatory cytokines IL-1beta and IL-18.

123 for maturation of the cytokines IL-1beta and IL-18.

124 nct from the pathway regulating IL-1beta and IL-18.

125 f the proinflammatory cytokines IL-1beta and IL-18.

126 f the proinflammatory cytokines IL-1beta and IL-18.

127 inflammatory cytokines, such as IL-1beta and IL-18.

128 leukin-1 (IL-1) family members, IL-1beta and IL-18.

129 -inflammatory mediators such as IL-1beta and IL-18.

130 matory cytokines, interleukin (IL)-1beta and IL-18.

131 ctivation and the production of IL-1beta and IL-18.

132 s independent of inflammasomes, IL-1beta and IL-18.

133 precursors into active forms of IL-1beta and IL-18.

134 n of proinflammatory cytokines, IL-1beta and IL-18.

135 f bioactive interleukin-1beta (IL-1beta) and IL-18 and inducing an inflammatory cell death called pyr

136 , including interleukin 1beta (IL-1beta) and IL-18.

137 e IL-1 superfamily, IL-1alpha, IL-1beta, and IL-18, in a range of conditions and cell types, includin

138 ; although elevated levels of ASC, IL-6, and IL-18 in patients' serum, and the response to anakinra,

139 of innate immune cytokines such as IL-8 and IL-18 along with more robust induction of non-classical

140 dChip), and circulating levels of hs-CRP and IL-18 were assessed in the association between anxiety a

141 e-I hyperactivation, cardiomyocyte death and IL-18 secretion were increased in T2DM mice.

142 ted inflammasome activation, cell death, and IL-18 secretion, suggesting that restoring mitophagy and

143 gnaling in adipose tissue from wild-type and IL-18(-/-) mice, but not IL-1beta(-/-) mice.

144 The upregulation of VEGF and IL-18 was detected in PDR.

145 X) signaling together with elevated YAP1 and IL-18 expression.

146 inary mRNA levels of renin, angiotensinogen, IL-18 and CTGF.

147 vivo by its naturally occurring antagonist, IL-18 Binding Protein (IL-18BP).

148 initiated by IL-36, but not IL-1alpha/beta, IL-18, or IL-33.

149 If the balance between IL-18 and IL-18BP is dysregulated, abnormal levels of fr

150 An interaction between IL-18 and severe anxiety with methylation of this CpG ci

151 related, and that IL-1R9 and IL-1R8 may bind IL-18.

152 regulated, abnormal levels of free bioactive IL-18 are detected, such as in the sera of Il-18bp knock

153 the IL-1 cytokine family, and elevated blood IL-18 concentrations associate with disease activity in

154 sion of IL-18R, which is a receptor for both IL-18 and IL-37, is also increased in the same brain are

155 ced in response to inflammatory stimuli, but IL-18 is constitutively expressed.

156 the NF-kappaB pathway, which is activated by IL-18 signaling.

157 of IL-18BP, excessive NK cell activation by IL-18 results in uncontrolled killing of human hepatocyt

158 specific plasma cells induced during chronic IL-18-mediated inflammation, as compared with IL-18 alon

159 Interestingly, both enzymes readily cleaved IL-18 and IL-33, two IL-1-related alarmins, as well as t

160 irst time demonstrated that IL-18BP counters IL-18 activation and therefore may mitigate/treat radiat

161 of 41 factors, including TNF, CCL5, CXCL10, IL-18, and IL-12 p40, and identified 140 drugs targeting

162 nal neurons produce the pleiotropic cytokine IL-18.

163 s to troponin I and proinflammatory cytokine IL-18.

164 Activation via the cytokine IL-18, a product of inflammasomes, gives rise to a rapid

165 Gene expression of proinflammatory cytokines IL-18 and IL-6 and phosphorylation of the endoplasmic re

166 as well as of the proinflammatory cytokines IL-18 and TNF, is increased in the amygdala and dorsolat

167 d by compromised secretion of cytoprotective IL-18 from IKKalpha-mutant intestinal epithelial cells b

168 Together, we show that neuron-derived IL-18 signaling controls tissue-wide intestinal immunity

169 of iNKT cells via cognate glycolipid during IL-18-mediated inflammation overrides the licensing func

170 These data establish IL-18 as a potent, independent, and modifiable driver of

171 Rather than impairing cytotoxicity, excess IL-18 acted on T lymphocytes to amplify their inflammato

172 otoxicity, specific viral infections, excess IL-18, and chimeric antigen receptor T-cell therapy.

173 In an adjuvant-induced MAS model, excess IL-18 promoted immunopathology, whereas perforin deficie

174 To determine the effects of excess IL-18 on virus-induced immunopathology, we infected Il18

175 Thus, excess IL-18 promotes hyperinflammation via an autoinflammatory

176 Despite being constitutively expressed, IL-18 expression was increased and sustained after stimu

177 ved that CD11c(+) dendritic cells expressing IL-18 are found in close proximity to ILC3s in human ton

178 ects in comparison to CAR T cells expressing IL-18 or IL-15.

179 portant roles for members of the IL-1 family-IL-18, IL-33, IL-36, IL-37, and IL-38-in inflammation an

180 s, we hypothesized that another receptor for IL-18 may exist, and that IL18BP is evolutionarily relat

181 , we discovered an intrinsic requirement for IL-18 signaling by splenic iNKT cells but not liver iNKT

182 of a monocyte and neutrophil-driven role for IL-18 in IBD pathogenesis.

183 MR analyses supported a causal role for IL-18 in inflammatory bowel disease (IBD) (P = 1.17 x 10

184 drugs with neither infection was tested for IL-18 by ELISA and for 16 other analytes by electrochemi

185 resulting in a radiation dose-dependent free IL-18 increase in these mice's serum which led to pathol

186 tio of IL-18/IL-18BP and decreasing the free IL-18 levels in irradiated mouse serum and significantly

187 o, Nlrc4(-/-) mice failed to produce gastric IL-18 upon H. pylori infection.

188 High IL-18 levels were correlated with detectable HIV viremia

189 g it a promising therapeutic target, but how IL-18 promotes hyperinflammation remains unknown.

190 However, how IL-18 and IL-1beta expression is regulated by different

191 Recent crystal structures of human IL-18 (hIL-18) in complex with its antagonists or cognat

192 We show that human IL-18 and IL-18BP are both secreted mostly by hepatocyte

193 They also show that human IL-18 is toxic to the liver and that IL-18BP is its anti

194 study regulatory mechanisms underlying human IL-18 expression.Methods: Samples from in vivo and in vi

195 We identified IL-18 as a cytokine that cooperates with an ILC3 surviva

196 loped incident HIV infection to determine if IL-18 increases with coinfection.

197 of inflammatory monocytes, were deficient in IL-18 production, and lacked NK cell-derived IFN-gamma.

198 findings reveal a fundamental difference in IL-18 and IL-1beta regulation and uncover novel mechanis

199 f IL-18, without a corresponding increase in IL-18-binding protein or IL-1beta, and their cells also

200 monocytes showed a significant reduction in IL-18, whereas IL-1beta was only reduced with ivacaftor/

201 Increased IL-18 levels in plasma and in induced skin blisters of D

202 HCV infected subjects resulted in increased IL-18 (p<0.001), while HIV suppression was associated wi

203 We assessed whether increased IL-18 could explain the increased incidence and progress

204 NLRP3-inflammasome signature with increased IL-18, IL-1beta, caspase-1 activity and ASC speck releas

205 acted on DCs by downregulating IL-15-induced IL-18 production, an important cytokine in NK cell activ

206 Moreover, H. pylori-induced IL-18 inhibits beta-defensin 1 expression in a NF-kappaB

207 ntified elevated signatures of inflammation (IL-18 and IL-6), lymphocytic and myeloid chemotaxis and

208 sed bioassay, we show that NSC80734 inhibits IL-18-induced production of IFN-gamma in a dose-dependen

209 lar S Typhimurium replication and initiating IL-18 secretion in mouse IECs but is dispensable in huma

210 ured five urine biomarkers of kidney injury (IL-18, NGAL, KIM-1, L-FABP, and albumin) and five plasma

211 e role of neuroimmune interactions involving IL-18 in enhancing susceptibility to medical illness (th

212 Synovial NK cell production of GM-CSF is IL-18-dependent.

213 (neutrophil gelatinase-associated lipocalin, IL-18, and kidney injury molecule-1 measured from donor

214 Despite lower IL-18, IFN-gamma was produced in similar amounts in wild

215 aspase-1 which cleaves pro-IL-18 into mature IL-18, leading to recruitment of interferon (IFN)-gamma-

216 Finally, LXR ligands further modulate IL-18 levels by inducing the expression of IL-18BP, a po

217 ll molecules can be identified that modulate IL-18 activity.

218 Main Results: Peripheral blood and monocytic IL-18 expression escaped LPS-induced immunoparalysis.

219 IL-1beta, and their cells also secreted more IL-18 but not IL-1beta in culture.

220 ll sequencing revealed that enteric neuronal IL-18 is specifically required for homeostatic goblet ce

221 regulatory mechanism that inhibits the NLRP6-IL-18 pathway in intestinal inflammation.

222 e HIV suppression was associated with normal IL-18 levels.

223 gocytes to directly enhance IL-1beta but not IL-18 secretion.

224 tein (IL-18BP) acts as a naturally occurring IL-18 decoy receptor.

225 mours and limits the anti-tumour activity of IL-18 in mice.

226 g protein (IL-18BP), a natural antagonist of IL-18, was significantly increased (1.7-63 fold) in mous

227 n-18 (IL-18) production, whereas blockade of IL-18 receptor in the brain helped protect against cereb

228 e mechanistic evidence for a contribution of IL-18 to inflammation and hyperinflammation in sepsis an

229 Strikingly, deletion of IL-18 from the enteric neurons alone, but not immune or

230 IRI promotes elaboration of IL-18 from endothelial cells to selectively expand allor

231 ent increase in renal cortical expression of IL-18, IL-1beta, and TGF-beta, despite a gradual decline

232 IFN signaling was essential for induction of IL-18 and macrophages lacking type I IFN signaling were

233 of IL-18BP, a potent endogenous inhibitor of IL-18.

234 fically target the rather large interface of IL-18 that is involved in extensive protein-protein inte

235 r myeloid cells, resulted in lower levels of IL-18 and a complete abrogation of NK cell function in H

236 murine macrophages produce reduced levels of IL-18 and are unable to optimally stimulate IFN-gamma pr

237 Deregulated levels of IL-18 are involved in the pathogenesis of multiple disor

238 gnature, as evidenced by increased levels of IL-18, IL-1beta, caspase-1 activity and ASC-speck releas

239 Patients had high serum levels of IL-18, without a corresponding increase in IL-18-binding

240 some complex and regulated the maturation of IL-18.

241 after treatment ended, with normalization of IL-18 and IL-1beta expression.

242 ic states characterized by overproduction of IL-18 and/or IL-22.

243 sistent joint inflammation via production of IL-18 and GM-CSF.

244 ntracellular S Typhimurium and production of IL-18 are dependent on caspase-4 in both transformed and

245 ion system are crucial for the production of IL-18 from human and murine gastric epithelial cells.

246 ith Burkholderia thailandensis Production of IL-18, but not IL-1beta, was decreased in Gsdmd(-/-) inf

247 of rhIL-18BP included balancing the ratio of IL-18/IL-18BP and decreasing the free IL-18 levels in ir

248 gether, our study identified a novel role of IL-18 in up-regulating nutrient transporters on NK cells

249 Notably, treatment of IL-18-stimulated NK cells with leucine activates the met

250 inflammasome activation and upregulation of IL-18 and IL-1beta It is not known if mitochondrial dama

251 Optimal NK cell responses were dependent on IL-18 and IL-12, whereas IFN-gamma secretion was restric

252 lls with cytokines, such as IL-15, IL-12, or IL-18, does not activate LFA-1 but increases the respons

253 bstantially rescued by exogenous IL-1beta or IL-18.

254 the production of the cytokines IL-1 and/or IL-18.

255 In (LPS/ATP-stimulated) PBMCs, IL-18/TNF/caspase-1 were all significantly decreased and

256 by human NK cells after NKG2D or IL-12 plus IL-18 stimulation and by mouse NK cells during mouse cyt

257 wing activation, especially after IL-12 plus IL-18 stimulation.

258 Cleavage of pro-interleukin (IL)-1beta, pro-IL-18, and gasdermin-D by activated caspase-1 resulted i

259 ream targets, including pro-IL-1beta and pro-IL-18 into their biologically active form.

260 pyroptosis and converts pro-IL-1beta and pro-IL-18 into their biologically active forms.

261 ory cytokine precursors pro-IL-1beta and pro-IL-18.

262 ptors activating caspase-1 which cleaves pro-IL-18 into mature IL-18, leading to recruitment of inter

263 ating the major pro-inflammatory factor, pro-IL-18.

264 ction-induced activation of the ATM-YAP1-pro-IL-18 pathway in epithelium is a key instigator of tissu

265 s, gastric epithelial cells can also produce IL-18.

266 in in medial habenula neurons, which project IL-18-containing axons to the interpeduncular nucleus.

267 ng were impaired in their ability to promote IL-18 induction.

268 Rationale: IL-18 is a member of the IL-1 cytokine family, and eleva

269 However, recombinant IL-18 previously did not demonstrate efficacy in clinica

270 whereas JAK/STAT inhibition strongly reduced IL-18 serum levels in two MAS mouse models and in a pati

271 s antibiotic treatment, dramatically reduces IL-18 and intestinal inflammation.

272 evolution, we engineered a 'decoy-resistant' IL-18 (DR-18) that maintains signalling potential but is

273 genes, and with high affinity to a separate IL-18 binding protein (IL-18BP).

274 Serum IL-18 and TNF decreased significantly with treatments, b

275 Serum IL-18 expression with or without JAK/STAT inhibition was

276 tion results in significantly elevated serum IL-18.

277 ed primary human monocytes revealed specific IL-18 expression kinetics controlled by IFNalpha/beta si

278 NLRC4 inflammasome activation and subsequent IL-18 production favors bacterial persistence by inhibit

279 Here, we demonstrate that IL-18 binding protein (IL-18BP), a natural antagonist of

280 Here, we demonstrate that IL-18 is a potent cytokine that can enhance the expressi

281 In this study, we found that IL-18 and IL-1beta are differentially regulated.

282 rent MAS.Conclusions: Our data indicate that IL-18 (but not IL-1beta) production from human monocytes

283 autoinflammatory murine model indicates that IL-18, the other cytokine triggered by inflammasome acti

284 We have reported that IL-18 plays an important role in radiation-induced injur

285 Our data suggest that IL-18 plays a key role in radiation-induced cell and tis

286 ur-infiltrating lymphocytes, suggesting that IL-18 therapy could enhance anti-tumour immunity.

287 eotide deletion in IL18BP, which encodes the IL-18 binding protein (IL-18BP).

288 Furthermore, IL-18BP treatment inhibited the IL-18 downstream target interferon (IFN)-gamma expressio

289 These results highlight the potential of the IL-18 pathway for immunotherapeutic intervention and imp

290 ient basophils had reduced expression of the IL-18 receptor, which impacted migration to lungs.

291 Among those, IL-18 is found highly upregulated in infected individual

292 ed responsiveness of FcRgamma(-) NK cells to IL-18 in particular, which was attributable to impaired

293 cell-mediated diseases, in sharp contrast to IL-18, which mainly regulates T(H)1 cell-mediated respon

294 lls with a diminished capacity to respond to IL-18 and to effectively modulate DC function may contri

295 ted donor-specific antibodies in response to IL-18 in vivo.

296 and could be expanded ex vivo in response to IL-18.

297 combined perforin deficiency and transgenic IL-18 production caused spontaneous hyperinflammation sp

298 Unlike wild-type IL-18, DR-18 exerted potent anti-tumour effects in mouse

299 erlies fulminant HAV hepatitis by unleashing IL-18.

300 L-18-mediated inflammation, as compared with IL-18 alone.