ライフサイエンスコーパス: pro-inflammatory

1 Potential pro-inflammatory 5-lipoxygenase (5-LOX) inhibition poten

2 anti-inflammatory mediator that antagonizes pro-inflammatory actions of FGF23 and TGF-beta.

3 ells, endosomal surplus of superoxide causes pro-inflammatory activation and TLR4 agonists act prefer

4 fraction significantly inhibited microglial pro-inflammatory activation by LPS, through the inhibiti

5 -dependent mechanisms, comprising attenuated pro-inflammatory activation of macrophages, impaired rec

6 regulate antimicrobial functions but exhibit pro-inflammatory activation only to type I IFNs.

7 the context, these hormones can also mediate pro-inflammatory activities, thereby serving as primers

8 eaved by few known proteases, modulating its pro-inflammatory activities.

9 or ELF3 and NFkappaB in the induction of the pro-inflammatory adipokine LCN2, providing additional ev

10 ynovial fibroblasts via raised levels of the pro-inflammatory adipokine leptin, leading to greater pr

11 In many different cell types, pro-inflammatory agonists induce the expression of cyclo

12 erleukin (IL)-6 that is known to induce both pro inflammatory and anti-inflammatory processes.

13 etion resulted in rapid deployment of both a pro-inflammatory and an immunosuppressive response in th

14 al cells with IL-33 led to the production of pro-inflammatory and angiogenic cytokines.

15 Endosteal AML cells produce pro-inflammatory and anti-angiogenic cytokines and gradu

16 LR4 by lipopolysaccharide (LPS) induces both pro-inflammatory and anti-inflammatory cytokine producti

17 The cyclooxygenase-2 is a pro-inflammatory and cancer marker, whose mRNA stability

18 3) and NFkappaB (nuclear factor kappaB), the pro-inflammatory and cancer-promoting transcription fact

19 nhibitor treatment down-regulated pathogenic pro-inflammatory and helper T cell 1 (Th1) responses and

20 ely, and large alveolar macrophages with low pro-inflammatory and phagocytic ability.

21 ial and small alveolar macrophages with more pro-inflammatory and phagocytic function respectively, a

22 on elevated pro-inflammatory signaling or by pro-inflammatory and pro-atherogenic microRNAs, miR-155

23 ted significantly increased expression of LV pro-inflammatory and pro-fibrotic genes and collagen dep

24 tion and reduced hepatic mRNA levels of both pro-inflammatory and pro-fibrotic genes.

25 g environmental cues to the acquisition of a pro-inflammatory, anti-tumor microenvironment in mouse b

26 lammation were linked to an overabundance of pro-inflammatory bacterial lineages and a lack of anti-i

27 Key pro-inflammatory canonical pathways induced by the LPS s

28 is critical to activate the particle-induced pro-inflammatory cascade in the peritoneum of mice.

29 also observed; because resistin is a potent pro-inflammatory compound, this decrease suggests that k

30 Interleukin-6 acts as both a pro-inflammatory cytokine and an anti-inflammatory myoki

31 ure to remifentanil reveals a suppression of pro-inflammatory cytokine and chemokine gene expression,

32 However, some pro-inflammatory cytokine and inflammasome-associated tr

33 However, LPS more potently induces pro-inflammatory cytokine and inflammasome-linked transc

34 Interleukin-18 (IL-18) is a pleiotropic pro-inflammatory cytokine belonging to the IL-1 superfam

35 ificantly reduced in vivo lung pathology and pro-inflammatory cytokine expression.

36 nockout (KO) attenuates colitis and inhibits pro-inflammatory cytokine expression.

37 and IL-36R was required for induction of the pro-inflammatory cytokine IL-17.

38 se 4, as well as a plasmatic increase of the pro-inflammatory cytokine IL-1beta.

39 ed receptor 2 and induces the release of the pro-inflammatory cytokine IL-6 from cells.

40 were found to secrete greater amounts of the pro-inflammatory cytokine IL-6, compared to those from n

41 IL-17 is a pro-inflammatory cytokine implicated a variety of autoim

42 sistent with TSP-1-enhanced phagocytosis and pro-inflammatory cytokine induction in cultured macropha

43 le particles with strong interferon and mild pro-inflammatory cytokine induction may qualify as vacci

44 d the synergistic negative regulation of the pro-inflammatory cytokine interferon-gamma (IFNgamma) an

45 L2 expression, while monocytes expressed the pro-inflammatory cytokine interleukin-1beta (IL-1beta).

46 THIK-1 function also inhibits release of the pro-inflammatory cytokine interleukin-1beta from activat

47 the biosynthesis of PGE2 and upregulation of pro-inflammatory cytokine interleukin-1beta.

48 11a KO mice show increased expression of the pro-inflammatory cytokine interleukin-6 (IL-6) relative

49 which resulted in increased concentration of pro-inflammatory cytokine levels in blood.

50 splay an age-related increase in circulating pro-inflammatory cytokine levels.

51 epithelial corneal integrity, and reduce the pro-inflammatory cytokine milieu in the tissue.

52 t not the OSPW-OF had significant effects on pro-inflammatory cytokine mRNA levels and cytokine prote

53 eine protease caspase-1, which activates the pro-inflammatory cytokine precursors pro-IL-1beta and pr

54 This anomaly was associated with excessive pro-inflammatory cytokine production as well as an incre

55 une responses and that tumor-induced central pro-inflammatory cytokine production can exist in the ab

56 Interpretation: Pro-inflammatory cytokine production had a dose-dependen

57 Higher Vdelta2 pro-inflammatory cytokine production was associated with

58 elevate GSH levels and attenuate LPS-induced pro-inflammatory cytokine production was inhibited by bu

59 uggest that peripheral tumors elicit central pro-inflammatory cytokine production, in turn leading to

60 -associated molecular pattern (PAMP)-induced pro-inflammatory cytokine production, inhibit NF-kappaB

61 A LipA-deficient strain induces heightened pro-inflammatory cytokine production, which is diminishe

62 associated with diminished Vdelta2(+) T cell pro-inflammatory cytokine production.

63 phenotype and an increased anti-inflammatory/pro-inflammatory cytokine ratio.

64 AMA0825 did not affect pro-inflammatory cytokine secretion from other ROCK-posi

65 JAK1 is a critical effector of pro-inflammatory cytokine signaling and plays important

66 is a key mediator of toll-like receptors and pro-inflammatory cytokine signaling pathways.

67 We specifically focus on the roles of pro-inflammatory cytokine signaling, peripheral monocyte

68 patients with hip OA exhibited differential pro-inflammatory cytokine signalling and peripheral and

69 ndent signaling that resulted in an elevated pro-inflammatory cytokine storm.

70 y target of Mi-2beta in keratinocytes is the pro-inflammatory cytokine thymic stromal lymphopoietin (

71 nged MDM showed ImI-mediated upregulation of pro-inflammatory cytokine TNF-alpha in an ImI concentrat

72 Moreover, we detected production of the pro-inflammatory cytokine TNF-alpha in cortical PLIN(+)

73 eukin 10 (IL-10), and decreasing that of the pro-inflammatory cytokine tumor necrosis factor (TNF).

74 Interleukin-17 (IL-17) is a critical pro-inflammatory cytokine, which has been demonstrated t

75 Interleukin-17 (IL-17) is a major pro-inflammatory cytokine: it mediates responses to path

76 people with DS display higher levels of many pro-inflammatory cytokines (e.g. IL-6, MCP-1, IL-22, TNF

77 ules (p-p65, ICAM-1, Cox-2, MMP3, and iNOS), pro-inflammatory cytokines (TNF-alpha, IL-1beta, IFN-gam

78 (MAIT) cells, as the most powerful source of pro-inflammatory cytokines after exposure to SAgs.

79 myeloid cells become hyperactivated, produce pro-inflammatory cytokines and act as more potent antige

80 elii nigeriensis N67C display high levels of pro-inflammatory cytokines and chemokines (IL-6, IFN-gam

81 ell responses, and the extended induction of pro-inflammatory cytokines and chemokines.

82 hallenged with LPS had exacerbated levels of pro-inflammatory cytokines and exhibited significantly w

83 uggest that the particles that do not induce pro-inflammatory cytokines and high levels of interferon

84 nd 4 weekly visits after MC were assayed for pro-inflammatory cytokines and HIV RNA.

85 vity and decreased LPS-induced production of pro-inflammatory cytokines and inducible nitric-oxide sy

86 virus specific antibodies, reduced levels of pro-inflammatory cytokines and innate immune cells.

87 elioidosis is associated with high levels of pro-inflammatory cytokines and is correlated with poor c

88 al cells and down-regulate the production of pro-inflammatory cytokines and nitric oxide (NO), in res

89 tion factors that regulate the expression of pro-inflammatory cytokines and other genes during the im

90 he immunoproteasome attenuates expression of pro-inflammatory cytokines and suppresses interferon-gam

91 are activated by - IL-31 with the release of pro-inflammatory cytokines and the induction of chemotax

92 PB significantly reduced the mRNA levels of pro-inflammatory cytokines and TLR-4 while increased tha

93 Pro-inflammatory cytokines are important mediators of is

94 lymphocyte infiltration and the secretion of pro-inflammatory cytokines are involved in the propagati

95 d lymphocyte content and low serum levels of pro-inflammatory cytokines as healthy controls; however,

96 ces the degrees of overproduction of ROS and pro-inflammatory cytokines both in vitro in RAW264.7 cel

97 n, which manifested as an increase in plasma pro-inflammatory cytokines compared to control mice.

98 is likely an effect of the overproduction of pro-inflammatory cytokines generated in MAVS-deficient m

99 Treatment of HDLECs with the pro-inflammatory cytokines IFN-gamma and TNF-alpha syner

100 so observed increased gene expression of the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-1bet

101 e activation of caspase-1 and the release of pro-inflammatory cytokines IL-1beta and IL-18 accompanie

102 al rupture of the cell causes release of the pro-inflammatory cytokines IL-1beta and IL-18, alarmins

103 vely suppress the production of ILC2-driven, pro-inflammatory cytokines IL-5 and IL-13.

104 ll as the repression of NF-kappaB, EDN-1 and pro-inflammatory cytokines IL-6, IL-12, and TNFalpha.

105 hosphorylation, the ISR and the induction of pro-inflammatory cytokines in human THP1 macrophages sub

106 Similarly, luteolin inhibits induction of pro-inflammatory cytokines in murine microglial macropha

107 thelial cells, HRVs induce the production of pro-inflammatory cytokines in PBMCs.

108 ing caries, dental pulp expresses a range of pro-inflammatory cytokines in response to the infectious

109 young, conventionally raised mice increases pro-inflammatory cytokines in the blood.

110 n anti-inflammatory cytokines and reduced in pro-inflammatory cytokines in treated mice.

111 leads to chloroquine sensitive production of pro-inflammatory cytokines including IL-1beta, while the

112 e 3' untranslated region (3'UTR) of numerous pro-inflammatory cytokines including IL-4, IL-13, IL-17

113 tor pathway leading to the generation of the pro-inflammatory cytokines interleukin-1beta and interle

114 Production of pro-inflammatory cytokines is reduced by ex vivo gene-si

115 tions of immune cells and elevated levels of pro-inflammatory cytokines predict poor prognosis.

116 ment of human MCF-7 breast cancer cells with pro-inflammatory cytokines results in ERalpha-dependent

117 posure of HAECs to oxidized phospholipids or pro-inflammatory cytokines results in signal-specific al

118 re driven by growth factors such as VEGF and pro-inflammatory cytokines such as TNF-alpha.

119 adhesion molecules and chemokines induced by pro-inflammatory cytokines such as TNFalpha and IFNgamma

120 ntly lower metabolic activity and release of pro-inflammatory cytokines than CFC tissue, but surprisi

121 fections by releasing cytotoxic granules and pro-inflammatory cytokines upon recognition of diseased

122 ed poorly with WT Tregs in vivo and produced pro-inflammatory cytokines upon stimulation.

123 A modest increase in pro-inflammatory cytokines was measured in the colons of

124 Results show pro-inflammatory cytokines were down-regulated significa

125 al and smooth muscle cells were treated with pro-inflammatory cytokines with or without aldosterone,

126 onments are typically hypercellular, rich in pro-inflammatory cytokines, and profoundly hypoxic.

127 h the induction of antiviral interferons and pro-inflammatory cytokines, but also by promoting cell d

128 her infections can control the expression of pro-inflammatory cytokines, but its role in melioidosis

129 lls occupy key cellular niches and elaborate pro-inflammatory cytokines, contributing to aging-relate

130 lammation play a role in potentiating PH and pro-inflammatory cytokines, including TNF, are associate

131 ciated with decreased serum concentration of pro-inflammatory cytokines, reduced neutrophil infiltrat

132 ter splanchnic nerve (GSN), and elevation of pro-inflammatory cytokines.

133 co-stimulatory signals and the secretion of pro-inflammatory cytokines.

134 trogen effects were partially overwhelmed by pro-inflammatory cytokines.

135 ammation process to the ISR and induction of pro-inflammatory cytokines.

136 are differently regulated by fluid flow and pro-inflammatory cytokines.

137 immunoisolated from FITC-mouse antibody and pro-inflammatory cytokines.

138 ctor-alpha and interleukin-1 beta, which are pro-inflammatory cytokines.

139 DARC) is an atypical receptor that regulates pro-inflammatory cytokines.

140 cell signaling, leading to the secretion of pro-inflammatory cytokines.

141 f regulation of activation of these cells by pro-inflammatory cytokines.

142 atients exhibit higher levels of circulating pro-inflammatory cytokines.

143 ional T-cell phenotype (Tconv) that secretes pro-inflammatory cytokines.

144 ell death, which coincides with the peaks of pro-inflammatory cytokines.

145 ynthesis provokes the production of specific pro-inflammatory cytokines.

146 Increases in mRNA level or stability of pro-inflammatory cytokines/chemokines are abolished by P

147 bone marrow, suppressing their production of pro-inflammatory/cytotoxic products while increasing the

148 f myeloid cells and diminished production of pro-inflammatory disease mediators including cytokines,

149 Here we report the pro-inflammatory effect of ImI, a well characterized con

150 panding allergen-specific Tregs and reducing pro-inflammatory effector T cells, these microparticles

151 H2-terminal kinase (JNK)-signaling cascades, pro-inflammatory effectors/cytokines, insulin resistance

152 he lungs, and the Asp358Ala variant may have pro-inflammatory effects in lung cells.

153 in sIL-6R shedding from neutrophils and its pro-inflammatory effects in the lung.

154 The cytotoxic and pro-inflammatory effects of studied NPs were investigate

155 artially responsible for the pro-oxidant and pro-inflammatory effects of uric acid.

156 itates metastasis by generating a senescent, pro-inflammatory endothelium.

157 rate (FDR)-corrected P = 0.25] but decreased pro-inflammatory Enterobacteriaceae (FDR-corrected P = 0

158 matory macrophages significantly reduced the pro-inflammatory environment and triggered a different h

159 Given that DED is characterized by a pro-inflammatory environment resulting in local tissue d

160 eration patients express increased levels of pro-inflammatory factors that can be normalized by the a

161 An important pro-inflammatory function of IL-6 trans-signaling is to

162 as well as to repress the expression of the pro-inflammatory gene eiger (TNF), a critical step to pr

163 H showed stronger suppression of LPS-induced pro-inflammatory gene expression compared with non-hydro

164 tivated in cancer cells, and correlates with pro-inflammatory gene expression in human cancers.

165 tio, NF-kappaB transcriptional activity, and pro-inflammatory gene expression in macrophages and micr

166 ks tumor necrosis factor alpha (TNFalpha) to pro-inflammatory gene expression in the nucleus.

167 ttenuating lipopolysaccharide- (LPS) induced pro-inflammatory gene expression in THP-1 macrophages.

168 sclerosis by activating growth-promoting and pro-inflammatory gene expression in vascular smooth musc

169 The pattern was reversed in the brain; pro-inflammatory gene expression increased among mice in

170 all interstitial macrophages had the highest pro-inflammatory gene expression levels, while large alv

171 ion of these enzymes correlated with splenic pro-inflammatory gene expression when treatment occurred

172 00 and the transcription factor NF-kappaB to pro-inflammatory gene promoters.

173 PARP14 silencing induces pro-inflammatory genes and STAT1 phosphorylation in M(IF

174 able to reduce the LPS-induced expression of pro-inflammatory genes IL-1beta, TNF-alpha and iNOS.

175 ypomethylation and overexpression of several pro-inflammatory genes such as COX2, IL8 and IL23R, sugg

176 d at ZT2 increased the expression of several pro-inflammatory genes within the spleen; this was not e

177 ot detected at GR transrepression sites near pro-inflammatory genes.

178 activating anti-inflammatory and repressing pro-inflammatory genes.

179 se cells produce IL-10 and downregulate some pro-inflammatory genes.

180 low impairs antibody class switching to the pro-inflammatory IgG2c antibody isotype by limiting the

181 d the IL-12 cytokine family as consisting of pro-inflammatory IL-12 and IL-23 and the anti-inflammato

182 ggregates and blunt macrophage apoptosis and pro-inflammatory IL-1beta levels, leading to reduced ath

183 caspase-1 to active caspase-1, which cleaves pro-inflammatory IL-1beta o mature IL-1beta causing infl

184 Our results indicate that EBI3 can promote pro-inflammatory IL-6 functions by mediating trans-signa

185 mized inverted ALI/postincubation procedure, pro-inflammatory immune responses, in terms of interleuk

186 s a critical role in host protection against pro-inflammatory insults.

187 AK to bovine cartilage explants, suppressing pro-inflammatory interleukin-6 (IL-6) expression after i

188 sessed inflammatory (im)balance by measuring pro-inflammatory interleukin-6 and anti-inflammatory int

189 singly, TAMs frequently co-express canonical pro-inflammatory (M1) and alternatively activated (M2) g

190 um of activation status, best exemplified by pro-inflammatory (M1) and anti-inflammatory (M2) phenoty

191 We found an increase in pro-inflammatory M1s in the small airways of NLFS and CO

192 g murine systemic infection, LipA suppresses pro-inflammatory macrophage activation, rendering these

193 s in male offspring, and increased number of pro-inflammatory macrophages emerged in VWAT along with

194 subtypes was unique during regeneration with pro-inflammatory macrophages failing to infiltrate the r

195 duced circulating inflammatory cytokines and pro-inflammatory macrophages in adipose tissue.

196 e 1 innate lymphoid cells (AT1-ILCs) promote pro-inflammatory macrophages in obesity, but little is k

197 strated by the decrease in the expression of pro-inflammatory markers and by the induction of a pro-r

198 nterest as growing literature indicates that pro-inflammatory markers can directly modulate affective

199 In the optic nerve, pro-inflammatory markers were upregulated within 6 hours

200 was not associated with increased levels of pro-inflammatory markers.

201 ny-stimulating factor (GM-CSF or Csf-2) is a pro-inflammatory mediator implicated in the pathogenesis

202 The pro-inflammatory mediator leukotriene B4 (LTB4) is impli

203 In MyD88(-/-) mice, this pro-inflammatory mediator-inducing ability was considera

204 usion and histopathology, reduces intrarenal pro-inflammatory mediators and salvages kidney function

205 coincided with the decrease of viral-induced pro-inflammatory mediators and viral-induced nuclear tra

206 nkrd26 down-regulation enhanced secretion of pro-inflammatory mediators by 3T3-L1 adipocytes as well

207 epsis states that an excessive production of pro-inflammatory mediators causes early deaths, whereas

208 The expression of pro-inflammatory mediators in peri-resection brain tissu

209 d type 2 diabetes, driving the production of pro-inflammatory mediators such as IL-1beta and IL-18.

210 ent reduces the expression of mTOR and other pro-inflammatory mediators, consequently slowing down mu

211 myeloperoxidase (MPO) and the expression of pro-inflammatory mediators.

212 increased accumulation and proliferation of pro-inflammatory metabolic M1-like macrophages highly ex

213 NAseq and protein level findings show that a pro-inflammatory microglial phenotype acquired in vitro

214 stic alpha7nAChR stimulation potentiates the pro-inflammatory microglial phenotype.

215 y CD8(+)T cells to the liver and exacerbated pro-inflammatory milieu.

216 (a) improves secretory function, (b) reduces pro-inflammatory molecule gene expression, (c) increases

217 regulation of microglial cell activation and pro-inflammatory molecule secretion, which may be import

218 the production of transcription factors and pro-inflammatory molecules and the activation of phospho

219 he effects of autophagy on the production of pro-inflammatory molecules in microglial cells and their

220 nd significantly elevated levels of multiple pro-inflammatory molecules.

221 ulocyte counts, along with the activation of pro-inflammatory monocyte subsets and release of inflamm

222 e, we show that glucose metabolism regulates pro-inflammatory NF-kappaB transcriptional activity thro

223 effects of DMF are facilitated by inhibiting pro-inflammatory NFkappaB, STAT3 and cJUN signaling, as

224 s endothelial dysfunction by suppressing the pro-inflammatory non-canonical TGF-beta pathway and by a

225 ted with A. terreus conidia neither produced pro-inflammatory nor T-cell stimulating cytokines.

226 ed in part by the constitutive activation of pro-inflammatory nuclear factor kappaB (NF-kappaB) signa

227 omic DNA serves as a reservoir to initiate a pro-inflammatory pathway in the cytoplasm in senescence

228 of the integrative stress response (ISR) and pro-inflammatory pathways.

229 ectory; an early protective peak and a later pro-inflammatory peak.

230 ion phenotype, which later change to a cidal pro-inflammatory phenotype as disease progresses and amy

231 ial proliferation that develops into a clear pro-inflammatory phenotype at late stages.

232 indicate that hypoxia promotes an eosinophil pro-inflammatory phenotype by enhancing eosinophil secre

233 a infected epithelial cells induced a potent pro-inflammatory phenotype in fibroblasts via an IL-1alp

234 ISA analyses showed that ER stress induced a pro-inflammatory phenotype in pancreatic normal, cancer

235 040(CC) allele skews memory T cells toward a pro-inflammatory phenotype involving Notch signaling, th

236 Similarly, soluble CTLA4 could reverse the pro-inflammatory phenotype of Aspergillus-induced regula

237 umulation of IL-6 in vesicles and an overall pro-inflammatory phenotype supported further by transcri

238 If so, anti-microglial agents targeting the pro-inflammatory phenotype would be most beneficial in t

239 in active lesions contained microglia with a pro-inflammatory phenotype, which expressed molecules in

240 stinct chemokine profile and a Th1-polarized pro-inflammatory phenotype.

241 increase in miR-21-5p expression promotes a pro-inflammatory phenotype.

242 but potently triggers IL-1beta release upon pro-inflammatory priming with phorbol ester or Toll-like

243 ride content (HTC) and hepatic expression of pro-inflammatory, pro-fibrotic and inflammasome genes.

244 Cyclooxygenase-2 (COX-2) triggers pro-inflammatory processes that can aggravate neuronal d

245 ession networks for acute-phase response and pro-inflammatory processes.

246 r Fibroblast Growth Factor (FGF) 23, a known pro-inflammatory, prognostic marker in chronic kidney di

247 factor networks that direct homeostatic and pro-inflammatory programs.

248 ble for deacylation of lipid A, reducing its pro-inflammatory property and resulting in polymyxin res

249 Calpains are ubiquitous pro-inflammatory proteases, whose activity is controlled

250 as a test subject to assess cytotoxicity and pro-inflammatory reactions to diatom-biosilica.

251 Medium chain fatty acids can activate the pro-inflammatory receptor GPR84 but so also can molecule

252 Thus, MPLA is a less potent activator of the pro-inflammatory response but retains effective immunomo

253 Two recent papers report the activation of a pro-inflammatory response by cytoplasmic DNA from aberra

254 irm that GSTO1-1 is critical for a TLR4-like pro-inflammatory response in vivo.

255 and permitted rapid progression from a skin pro-inflammatory response to a lethal systemic condition

256 -1 with TLR8(+) early endosomes, triggered a pro-inflammatory response, and inhibited trans-infection

257 ults indicate that mineral particles promote pro-inflammatory responses by engaging neutrophils and m

258 play to enhance viral resistance and induce pro-inflammatory responses essential for confronting inf

259 thors show that glucose metabolism regulates pro-inflammatory responses through effects on the cytoso

260 for the first time that di-C18 LPAs trigger pro-inflammatory responses through Toll-like receptor 2

261 addition to their well-characterized role in pro-inflammatory responses, keratinocytes also directly

262 f terminal cell-cycle arrest associated with pro-inflammatory responses.

263 These data indicate a pro-inflammatory role for Ang-1 with respect to neutroph

264 TO1-1) is an atypical GST reported to play a pro-inflammatory role in response to LPS.

265 rized by a permanent cell-cycle arrest and a pro-inflammatory secretory phenotype, and can be induced

266 t continue to characterize the specific role pro-inflammatory signaling in the maintenance of these u

267 ive, mechanistically precise interception of pro-inflammatory signaling mediated by reactive oxygen s

268 afB is strongly down-regulated upon elevated pro-inflammatory signaling or by pro-inflammatory and pr

269 uitin coat, which serve as antibacterial and pro-inflammatory signalling platforms.

270 ) stress responses essentially contribute to pro-inflammatory signalling.

271 alyses, we suggest a pan-cancer mechanism of pro-inflammatory signals from the tumor stimulates an in

272 ned IFN-gamma and TNF-alpha are the dominant pro-inflammatory signals linking atherosclerosis and pso

273 cell wall breakdown, limits the induction of pro-inflammatory signals required for optimal Th17 polar

274 s exhibit features of senescence and produce pro-inflammatory signals that promote their clearance by

275 unity likely occurs through the dampening of pro-inflammatory signals upon engulfment of dying cells

276 Our results show that MEHP can induce a pro-inflammatory state in differentiated adipocytes.

277 ing Notch signaling, provoke a senescent and pro-inflammatory state in endothelial cells, promoting n

278 We have previously shown that in a pro-inflammatory state, a decrease in membrane channel e

279 Pro-inflammatory stimuli lead to endothelial inflammatio

280 Here the authors show that pro-inflammatory stimuli lead to endothelial inflammatio

281 Pro-inflammatory stimuli led to increased endothelial CD

282 Activation of the endothelium by pro-inflammatory stimuli plays a key role in the pathoge

283 we first showed that macrophages exposed to pro-inflammatory stimuli released TRX in sufficient quan

284 EC identity and their specific responses to pro-inflammatory stimuli.

285 xpression, and was induced in cartilage by a pro-inflammatory stimulus.

286 as a potential therapeutic target to reduce pro-inflammatory stress.

287 ewed polarization of naive T cells towards a pro-inflammatory T helper (TH17) cell state and away fro

288 L-12 family cytokine, plays pivotal roles in pro-inflammatory T helper 17 cell responses linked to au

289 ppressor cells of the immune system, control pro-inflammatory T-cell responses, but can also contribu

290 hese patients are associated with persistent pro-inflammatory T-helper (TH)2 and TH17 responses.

291 gnificantly enriched in LTBI; in contrast to pro-inflammatory Th17 cells (IFNgamma(+)IL17A(+)/IL10(-)

292 mportantly, TRAILPEG decreased the number of pro-inflammatory Th17 cells in inflamed arthritic joints

293 es of immune-suppressive regulatory T cells, pro-inflammatory Th17 cells, or their ability to express

294 ults define the molecular signature of human pro-inflammatory TH17 cells, which can be used to both i

295 This drives growth and pro-inflammatory TH17 over anti-inflammatory-induced T r

296 nstrate that these regulatory T-cells with a pro-inflammatory TH17-like phenotype can be reprogrammed

297 suggest a role for regulatory T-cells with a pro-inflammatory TH17-like phenotype in Aspergillus-asso

298 also contribute to disease by shifting to a pro-inflammatory TH17-like phenotype.

299 nt mechanism involves tethering of GR to the pro-inflammatory transcription factor activator protein-

300 dative transformation potently inhibited the pro-inflammatory transcription factor nuclear factor kap