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 inhibited goblet cell maturation by regulating the

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 recognized as binding to the protein products o

7 IL-18 levels and MAIT cell activation correlate with dis

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 showed synergy with IL-7 and enhanced proliferatio

12 IL-18 was significantly elevated in coinfected individua

13 in (NGAL), kidney injury molecule-1 (KIM-1), IL-18, and liver-type fatty acid binding protein (L-FABP

14 in (NGAL), kidney injury molecule-1 (KIM-1), IL-18, and liver-type fatty acid binding protein (L-FABP

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

16 arious signaling pathways initiated by IL-1, IL-18, and toll-like receptors, the precise contribution

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

18 during NK stimulation with cytokines (IL-12, IL-18, and IL-15).

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

20 The production of interleukin 15 (IL-15), IL-18, gamma interferon (IFN-gamma), granulocyte colony-

21 ctivation, augmented levels of IL-12, IL-15, IL-18, IFN-gamma, and TNF were detected in patient plasm

22 Interleukin 18 (IL-18) promotes atherosclerotic plaque formation and is

23 ed to a greater reduction in interleukin-18 (IL-18) (-7.0% +/- 2.8% compared with -0.5% +/- 3.0%, res

24 tein 1 beta (MIP-1beta), and interleukin-18 (IL-18) in 131 patients with chronic HCV treated with sof

25 Interleukin-18 (IL-18) is a pleiotropic cytokine centrally involved in t

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

27 ich was mediated by impaired interleukin-18 (IL-18) signaling.

28 the proinflammatory cytokine interleukin-18 (IL-18) was significantly higher in PVAN biopsies compare

29 tified a protective role for interleukin-18 (IL-18).

30 sting evidence suggests that interleukin-18 (IL-18; an IL-1 family cytokine) is elevated in depressio

31 equently suppresses the release of IL-1beta, IL-18 and HMGB1 by macrophages.

32 nt is dependent on the presence of IL-1beta, IL-18, and caspase-1.

33 caspase-1 cleavage but suppresses IL-1beta, IL-18, and other cytokines and chemokines.

34 ent release of biologically active IL-1beta, IL-18, and other soluble mediators of inflammation.

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

36 and YopM induces elevated levels of IL-1beta/IL-18 in vitro and in vivo and is significantly attenuat

37 both exert a tight control of host IL-1beta/IL-18 production to benefit the bacteria, resulting in a

38 m of influences by YopJ and YopM on IL-1beta/IL-18 release is suppressive.

39 me is responsible for QS-21-induced IL-1beta/IL-18 release.

40 In the context of IL-1beta/IL-18 secretion, however, in vitro studies indicate that

41 e anti-microbial effects induced by IL-1beta/IL-18, it may be desirable for pathogens to manipulate t

42 educed in Aim2-deficient mice in an IL-1beta/IL-18-independent manner after DNA vaccination.

43 this study, the authors believe that TLR-4, IL-18, and uric acid could have a role in the inflammato

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

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

46 Caspase-1-activated IL-18 induces IFN-gamma to prime caspase-11 and rapidly

47 ver, did not induce the processing to active IL-18, suggesting a two-step regulation of IL-18 in thes

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

49 Additionally, IL-18 processing of its precursor inactive form to its b

50 Although IL-18 exerted pathogenic functions during ileitis trigge

51 Although IL-18 has not previously been shown to promote T lymphop

52 Thus, an IL-18-MyD88 signaling axis facilitates the prolific expa

53 robust caspase-1 activation and triggers an IL-18-dependent proinflammatory response.

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

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

56 lammatory cytokines interleukin-1 (IL-1) and IL-18 show an age-dependent regulation implicating infla

57 revalent KTRs, higher urine NGAL, KIM-1, and IL-18 levels independently and differentially associated

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

59 eased functional responsiveness to IL-12 and IL-18, as well as to K562 cells, indicating that the NK

60 n BCG stimulation was dependent on IL-12 and IL-18.

61 in response to elevated levels of IL-12 and IL-18.

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

63 Cytokines such as interleukin 12 (IL-12) and IL-18 are critical regulators of NK cell activation, but

64 Interleukin 12 (IL-12) and IL-18 regulated this conversion, and during viral infect

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

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

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

68 ivation with the cytokines IL-12, IL-15, and IL-18 or in response to antigens or cytomegalovirus (CMV

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

70 cellular release of IL-1beta, IL-1alpha, and IL-18, that CP-456,773 prevents inflammasome activation

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

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

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

74 ncreased cellular production of IL-1beta and IL-18 and higher circulating levels of both cytokines.

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

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

77 f the proinflammatory cytokines IL-1beta and IL-18 and the initiation of an inflammatory cell death p

78 nt) processing and secretion of IL-1beta and IL-18 are critical events at the interface of the bacter

79 vation and further secretion of IL-1beta and IL-18 by P. brasiliensis-infected macrophages.

80 e-1 activation and secretion of IL-1beta and IL-18 from mouse macrophages and human peripheral blood

81 hereby, reducing the release of IL-1beta and IL-18 in human inflammatory cells after NALP3 activation

82 a demonstrate the production of IL-1beta and IL-18 in KC, suggesting that KC contain functional infla

83 c lesions and also higher serum IL-1beta and IL-18 in Ogg1(-/-)Ldlr(-/-) mice than in Ldlr(-/-).

84 sis and decreased production of IL-1beta and IL-18 in response to LPS challenge.

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

86 of infection, are required for IL-1beta and IL-18 processing and release.

87 background exhibited defective IL-1beta and IL-18 production at the infection site and were resistan

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

89 ammasome-mediated interleukin (IL)-1beta and IL-18 production in human monocytes.

90 m inflammasomes and to regulate IL-1beta and IL-18 production in myeloid cells.

91 esterol crystals did not induce IL-1beta and IL-18 production in Nlrp3(-/-) macrophages.

92 activation and in interleukin (IL)-1beta and IL-18 production, and there was improved survival in a m

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

94 ding to the secretion of mature IL-1beta and IL-18 proteins.

95 1 to elicit caspase-1-dependent IL-1beta and IL-18 release in antigen-presenting cells such as macrop

96 ered with caspase-1 activation, IL-1beta and IL-18 release, pyroptosis, and the release of ASC partic

97 , ureB mutants failed to induce IL-1beta and IL-18 secretion and to promote Treg responses.

98 this fungus suppresses interleukin-1beta and IL-18 secretion by inhibiting both canonical and non-can

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

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

101 ese cells primed skin to induce IL-1beta and IL-18 signaling, which further promoted the cytokines IF

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

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

104 f the proinflammatory cytokines IL-1beta and IL-18, and a form of cell death termed pyroptosis.

105 rgets (e.g., dual inhibition of IL-1beta and IL-18, and coadministration of endothelial progenitor ce

106 tissues, reduced production of IL-1beta and IL-18, and consequently dampened activation of effector

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

108 ncludes secretion of cytokines, IL-1beta and IL-18, and induction of an inflammatory form of cell dea

109 and production of interleukin (IL)-1beta and IL-18, as well as induction of AIM2-dependent and stimul

110 f the proinflammatory cytokines IL-1beta and IL-18, as well as to induce pyroptotic cell death in res

111 f the proinflammatory cytokines IL-1beta and IL-18, but it has not yet been determined whether human

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

113 f the proinflammatory cytokines IL-1beta and IL-18, can be inhibited by ethanol, and we sought to bet

114 inflammatory cytokines, such as IL-1beta and IL-18, markers of inflammasome activation also increased

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

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

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

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

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

120 te immune response initiated by IL-1beta and IL-18.

121 the pro-inflammatory cytokines IL-1beta and IL-18.

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

123 and secretion of interleukin (IL)-1beta and IL-18.

124 of caspase-1 and the release of IL-1beta and IL-18.

125 P3 expression and production of IL-1beta and IL-18.

126 caspase-1 and the secretion of IL-1beta and IL-18.

127 e the proinflammatory cytokines IL-1beta and IL-18.

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

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

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

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

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

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

134 amounts of interleukin-1beta (IL-1beta) and IL-18 and had a defect in NLRC4 inflammasome oligomeriza

135 cytokines, interleukin-1beta (IL-1beta) and IL-18, and cell death.

136 neration of interleukin-1beta (IL-1beta) and IL-18, and pyroptotic cell death.

137 release of interleukin-1beta (IL-1beta) and IL-18, and several inflammasomes protect against intesti

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

139 y cytokines interleukin-1beta (IL-1beta) and IL-18.

140 y cytokines interleukin-1beta (IL-1beta) and IL-18.

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

142 Interferons, IL-1beta, and IL-18 are also implicated in autoimmune disease and chro

143 Mean IP-10, MCP-1, MIP-1beta, and IL-18 levels all decline on therapy, but display differe

144 (-/-), TLR4(-/-), TLR9(-/-), IL-1R(-/-), and IL-18(-/-) mice, we found that, while the knockout of a

145 re observed in plasma and salivary TLR-4 and IL-18 levels, along with clinical measurements such as p

146 TLR-4 and IL-18 measurements were done using commercially availabl

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

148 nes, such as IFN-gamma, TNF-alpha, IL-6, and IL-18.

149 activation leading to caspase-1 cleavage and IL-18 secretion, which contribute to development of fata

150 clinical variables and anuria, clusterin and IL-18 independently enhanced the clinical model for pred

151 Urine KIM-1/creatinine and IL-18/creatinine independently associated with greater r

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

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

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

155 ts of vascular endothelial growth factor and IL-18 showed an opposite evolution of vascular endotheli

156 h levels of secreted IL-1beta (fivefold) and IL-18 (10-fold) when stimulated with 1,000-fold less LPS

157 Monocytes and IL-18, a signature cytokine of inflammasome activation,

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

159 ntified strong associations between baseline IL-18 and mu-opioid receptor availability in major depre

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

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

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

163 hmatic subjects with low nasal and bronchial IL-18 levels.

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

165 tion in mature macrophages is unaltered, but IL-18 production from monocytes is greatly exaggerated,

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

167 e results indicate that the TLR2/NLRP3/CASP1/IL-18 axis is critical to H. pylori-specific immune regu

168 hat experimental mood induction would change IL-18, the extent proportional to opioid neurotransmitte

169 Circulating IL-18 concentrations are associated with type 2 diabetes

170 entify causal variants affecting circulating IL-18 concentrations, we applied various omics and molec

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

172 Conversely, IL-18 was required for the expression of IL-22 in innate

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

174 The proinflammatory cytokine IL-18 has central anorexigenic effects and was proposed

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

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

177 pro-inflammatory IL-1 superfamily cytokine, IL-18, and its relationship to mu-opioid neurotransmissi

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

179 Our results define IL-18 as an IL-22 target gene in epithelial cells and de

180 Epithelial-derived IL-18 promotes dendritic cell-driven Th1 and Th17 immuni

181 on of the deleterious and tissue-destructive IL-18/IL-1/IL-17A axis represents a novel therapeutic ap

182 ing NLRP6 inflammasome signaling, epithelial IL-18 secretion, and downstream anti-microbial peptide (

183 Exogenous IL-18 enhanced the gammadelta T cell expansion with all

184 suggested a therapeutic approach: exogenous IL-18 restored perforin-dependent cytotoxicity during in

185 delta T cells, whereas addition of exogenous IL-18 restored the IFN-gamma response of gammadelta T ce

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

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

188 the importance of the NLRC4 inflammasome for IL-18 production in acute coronary syndrome patients.

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

190 To assess a potential role for IL-18 in T cell development, we sort-purified mouse bone

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

192 8Ralpha (Il18ra(-/-)), which lack functional IL-18 receptors.

193 ound that both subunits of the heterodimeric IL-18 receptor are highly expressed in the BST and that

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

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

196 complex known as the inflammasome; however, IL-18 has not yet been specifically implicated in the pa

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

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

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

200 Th17 responses and gastric immunopathology, IL-18 is required for Treg differentiation, H. pylori pe

201 Results showed mood induction impacted IL-18 (F2,25=12.2, P<0.001), sadness increasing IL-18 (T

202 The impaired IL-18 levels observed are shown to result in reduced int

203 In depressed volunteers, changes in IL-18 were more pronounced (F2,25=3.6, P=0.03) and linea

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

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

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

207 iants explained 8% of the total variation in IL-18 levels in the cohort.

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

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

210 18 (F2,25=12.2, P<0.001), sadness increasing IL-18 (T27=2.6, P=0.01) and neutral mood reducing IL-18

211 Indeed, IL-18 administration in sepsis increased IL-17A producti

212 s the host epithelial inflammasome to induce IL-18 release.

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

214 Instead, the inflammasome-IL-18 pathway impacted maturation of hepatic NK cells, s

215 In conclusion, LXR activation inhibits IL-18 production through regulation of its transcription

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

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

218 Interestingly, IL-18-sensitve Type III neurons were recorded in the jux

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

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

221 onocytes in culture is associated with lower IL-18 levels in culture supernatant and diminished produ

222 g cells in response to inflammatory mediator IL-18 or alarmin IL-33, but not by TCR signaling that is

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

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

225 ignals from the system and prevents monocyte IL-18 production.

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

227 itatory input on Type III GABAergic neurons, IL-18 can increase the firing of glutamatergic LH neuron

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

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

230 ges (SCMsmall ef, Cyrillic) or abrogation of IL-18 signaling dramatically impairs the Ag-specific B c

231 stromal layers in the presence or absence of IL-18 and/or IL-7.

232 In the absence of IL-18, bacterial burdens persist, eventually triggering

233 demonstrate elevated serum concentrations of IL-18 compared with adults.

234 Thus, we determined the contribution of IL-18 to lethality and its mechanism in a murine model o

235 17A is a previously unrecognized effector of IL-18-mediated injury in neonatal sepsis and that disrup

236 The effects of IL-18 are cell-specific and were observed in Type III bu

237 Effects of IL-18 were mediated by the IL-18R because they were abse

238 e LPS-induced mRNA and protein expression of IL-18 in bone marrow-derived macrophages.

239 Tubular expression of IL-18 was significantly increased in PVAN compared with

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

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

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

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

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

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

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

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

248 Neutralization of IL-18 abrogated protection in susceptible recipient mice

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

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

251 This novel regulation of IL-18 by LXR could be applied to modulate the severity o

252 e IL-18, suggesting a two-step regulation of IL-18 in these cells.

253 cells and underscores the important role of IL-18 in driving gammadelta T cell expansion.

254 chanisms involving insufficient secretion of IL-18, but not IL-12 or IL-15 and/or induction of NK cel

255 could be applied to modulate the severity of IL-18 driven metabolic and inflammatory disorders.

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

257 gulation-is TCR-independent but dependent on IL-18 in synergy with IL-12, IL-15 and/or interferon-alp

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

259 Plasma IL-18 levels pre-cART correlated inversely with NO level

260 ntally induced mood (sad, neutral) on plasma IL-18 and relationships with concurrent changes in the c

261 more robust in vitro responses to IL-12 plus IL-18 and RL Ag, indicating that MR1 is necessary for th

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

263 performed spontaneously or after IL-12 plus IL-18 stimulation in the presence of K562 or P815 target

264 sence of cirrhosis and elevated pretreatment IL-18.

265 pro-interleukin-1beta (pro-IL-1beta) and pro-IL-18 and drive pyroptosis.

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

267 and caspase 8-mediated pro-IL-1beta and pro-IL-18 processing in bone marrow-derived dendritic cells

268 eads to the cleavage of pro-IL-1beta and pro-IL-18, as well as the subsequent release of biologically

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

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

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

272 the innate immune responses, including rapid IL-18 production, induced by GLA-SE.

273 BST and that local injection of recombinant IL-18 (50 ng/ml) significantly reduced c-fos activation

274 ) myeloid cells, and blocking IL-17A reduced IL-18-potentiated mortality to both neonatal sepsis and

275 (T27=2.6, P=0.01) and neutral mood reducing IL-18 (T27=-4.1, P<0.001).

276 m polymicrobial sepsis, whereas replenishing IL-18 increased lethality to sepsis or endotoxemia.

277 rticle, we demonstrate that NK cells require IL-18 signaling to generate a robust primary response du

278 IFN-gamma by these cell populations required IL-18, sensing of mycobacterial viability, Mtb protein 6

279 However, salivary IL-18 levels rose up to > 5-fold in the patients with CP

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

281 tion results in significantly elevated serum IL-18.

282 In contrast, in TCMR, IL-18 was expressed predominantly by CD163-positive macr

283 ffects T lymphopoiesis and demonstrated that IL-18 can positively impact bone marrow lymphopoiesis an

284 formed in BST brain slices demonstrated that IL-18 strongly reduces the excitatory input on BST neuro

285 in TB-IRIS patients, providing evidence that IL-18 is a marker of inflammasome activation.

286 We find that IL-18-null neonatal mice are highly protected from polym

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

288 e we tested in the mouse the hypothesis that IL-18 can decrease food intake by acting on neurons of t

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

290 bal microarray meta-analysis prediction that IL-18 affects T lymphopoiesis and demonstrated that IL-1

291 In conclusion, our data show that IL-18 may inhibit feeding by inhibiting the activity of

292 , which mediates signaling downstream of the IL-18 and IL-1 receptors.

293 tive contribution of genetic variants to the IL-18 levels has not been fully determined.

294 ria terminalis to reduce food intake via the IL-18 receptor.

295 This cytokine is activated identically to IL-18 by an intracellular protein complex known as the i

296 stemic autoinflammation that is reduced when IL-18 is deleted but not when IL-1 signaling is removed.

297 infected AGM milk than in that of RMs, while IL-18 and IL-6 trended significantly higher in SIV-infec

298 5 chromosomal regions, were associated with IL-18 levels (minimum P=6.99x10(-72)).

299 ular endothelial growth factor compared with IL-18 concentrations, suggesting that they regulate each

300 E adjuvant operates through interaction with IL-18-producing SCMsmall ef, Cyrillic for the rapid indu