ライフサイエンスコーパス: inflammatory cytokine

1 omers while modestly reduced the level of an inflammatory cytokine.

2 lls or spleen-derived endothelial cells with inflammatory cytokines.

3 g B cells to proliferate and produce Abs and inflammatory cytokines.

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

5 esis provokes the production of specific pro-inflammatory cytokines.

6 aB activation and enhanced the production of inflammatory cytokines.

7 y inducing their migration and expression of inflammatory cytokines.

8 g responses via inducible production of anti-inflammatory cytokines.

9 stimulatory signals and the secretion of pro-inflammatory cytokines.

10 f Foxp3 and were more stable when exposed to inflammatory cytokines.

11 en in vivo, TRIM21 impacted the secretion of inflammatory cytokines.

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

13 en effects were partially overwhelmed by pro-inflammatory cytokines.

14 tion process to the ISR and induction of pro-inflammatory cytokines.

15 exhibited significantly increased levels of inflammatory cytokines.

16 r expression and production of pro- and anti-inflammatory cytokines.

17 differently regulated by fluid flow and pro-inflammatory cytokines.

18 H3K4me3 at inflammatory gene promoters, and inflammatory cytokines.

19 unoisolated from FITC-mouse antibody and pro-inflammatory cytokines.

20 cy correlated significantly with circulating inflammatory cytokines.

21 ages, Treg lymphocytes, oxidative stress and inflammatory cytokines.

22 ayer tension and permeability in response to inflammatory cytokines.

23 were a host of circulating or intra-alveolar inflammatory cytokines.

24 Ralpha that inhibits expression/secretion of inflammatory cytokines.

25 ed by endothelial cells under the control of inflammatory cytokines.

26 nts exhibit higher levels of circulating pro-inflammatory cytokines.

27 l T-cell phenotype (Tconv) that secretes pro-inflammatory cytokines.

28 tivation, impacting production of downstream inflammatory cytokines.

29 matopoietic cells, even when pretreated with inflammatory cytokines.

30 ith arachidonic acid increased expression of inflammatory cytokines, 12-hydroxy-eicosatetraenoic acid

31 ression, genomic amplification combined with inflammatory cytokine activation of ADAR1 could stimulat

32 T) cells, as the most powerful source of pro-inflammatory cytokines after exposure to SAgs.

33 erence tomography), expression of 3 of these inflammatory cytokines, all previously implicated in the

34 to remifentanil reveals a suppression of pro-inflammatory cytokine and chemokine gene expression, con

35 , higher brain viral loads, and higher brain inflammatory cytokine and chemokine levels than control

36 foreign body giant cell (FBGC) formation and inflammatory cytokine and chemokine secretion.

37 ription factors previously shown to regulate inflammatory cytokine and effector molecule production.

38 Interleukin-1beta (IL-1beta), an inflammatory cytokine and IL-1 receptor ligand, has dive

39 However, some pro-inflammatory cytokine and inflammasome-associated transc

40 However, LPS more potently induces pro-inflammatory cytokine and inflammasome-linked transcript

41 and IRF2 to the Tlr3 promoter, without which inflammatory cytokine and type I IFN responses to the do

42 oid cells become hyperactivated, produce pro-inflammatory cytokines and act as more potent antigen pr

43 Biomarkers of inflammation such as inflammatory cytokines and acute-phase proteins are reli

44 cardiomyopathy, as well as the expression of inflammatory cytokines and apoptotic proteins.

45 (-/-)PS mice, and there were lower levels of inflammatory cytokines and astrogliosis.

46 ually by treatment with antibodies targeting inflammatory cytokines and by the administration of bene

47 nigeriensis N67C display high levels of pro-inflammatory cytokines and chemokines (IL-6, IFN-gamma,

48 resulted in decreased cardiac expression of inflammatory cytokines and chemokines and decreased infl

49 It inhibited the expression of inflammatory cytokines and chemokines in macrophages and

50 odies, increasing concentration and range of inflammatory cytokines and chemokines, and altered metab

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

52 e in the innate immune response by secreting inflammatory cytokines and chemokines.

53 ing MPs in CF disease have a high content of inflammatory cytokines and could increase osteoclast dif

54 lyphaga 50372 led to increased production of inflammatory cytokines and cytopathic effects visible un

55 lammasome responses and excessive release of inflammatory cytokines and danger signals are linked to

56 ll infiltration, despite suppression of some inflammatory cytokines and delayed wound healing.

57 enged with LPS had exacerbated levels of pro-inflammatory cytokines and exhibited significantly worse

58 tion and fibrosis with the downregulation of inflammatory cytokines and fibrotic gene expressions.

59 ent Progenitor cells, contains multiple anti-inflammatory cytokines and growth factors.

60 st that the particles that do not induce pro-inflammatory cytokines and high levels of interferons ca

61 ection, exhibiting decreased levels of serum inflammatory cytokines and higher parasite burden in the

62 iated by TLR4, as we found less secretion of inflammatory cytokines and higher secretion of anti-infl

63 weekly visits after MC were assayed for pro-inflammatory cytokines and HIV RNA.

64 and decreased LPS-induced production of pro-inflammatory cytokines and inducible nitric-oxide syntha

65 s specific antibodies, reduced levels of pro-inflammatory cytokines and innate immune cells.

66 idosis is associated with high levels of pro-inflammatory cytokines and is correlated with poor clini

67 This influenced plasma concentration of inflammatory cytokines and key metabolic hormones consid

68 viremia were similar, however, the levels of inflammatory cytokines and MDSC were more pronounced pos

69 ammatory phenotype characterized by elevated inflammatory cytokines and myeloproliferation.

70 late human whole blood cells to release anti-inflammatory cytokines and neurotrophins.

71 ells and down-regulate the production of pro-inflammatory cytokines and nitric oxide (NO), in respons

72 factors that regulate the expression of pro-inflammatory cytokines and other genes during the immune

73 lial cells revealed differential response to inflammatory cytokines and other RNABPs.

74 ersely, CTRP6 deficiency reduced circulating inflammatory cytokines and pro-inflammatory macrophages

75 al immunity remodeled with increased in anti-inflammatory cytokines and reduced in pro-inflammatory c

76 ted prior to the increase of blood levels of inflammatory cytokines and stress-related hormones.

77 mmunoproteasome attenuates expression of pro-inflammatory cytokines and suppresses interferon-gamma-d

78 significantly reduced the mRNA levels of pro-inflammatory cytokines and TLR-4 while increased that of

79 Blockade of CB1 attenuated DIO, inflammatory cytokines and trafficking of M1 macrophages

80 Myeloid cells produced more inflammatory cytokines and upregulated MHCII.

81 e leukocytosis, elevated serum pro- and anti-inflammatory cytokines, and evidence of innate cell acti

82 means, reduced amyloid burden, the levels of inflammatory cytokines, and memory deficits.

83 Indeed, inflammatory cytokines are implicated in synaptic dysfun

84 Pro-inflammatory cytokines are important mediators of islet

85 hocyte infiltration and the secretion of pro-inflammatory cytokines are involved in the propagation o

86 Inflammatory cytokines are known to play a key role in r

87 respiratory distress syndrome, pro- and anti-inflammatory cytokines are strongly associated with mort

88 mphocyte content and low serum levels of pro-inflammatory cytokines as healthy controls; however, don

89 atory phenotype, with increased secretion of inflammatory cytokines as well as chemokines.

90 nctioned as a negative regulator of multiple inflammatory cytokines, as IL-1alpha, IL-1beta, IL-6, IL

91 was implicated as a checkpoint regulator of inflammatory cytokines, as well as an inflammasome activ

92 modulate DC function, enhancing secretion of inflammatory cytokines at very low doses, and suppressin

93 the level of reactive oxygen species (ROS), inflammatory cytokines, autophagy, and DNA damage.

94 ocytes and dendritic cells that produce more inflammatory cytokines both at baseline and following en

95 the degrees of overproduction of ROS and pro-inflammatory cytokines both in vitro in RAW264.7 cells a

96 e induction of antiviral interferons and pro-inflammatory cytokines, but also by promoting cell death

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

98 were strongly associated with cervicovaginal inflammatory cytokines, but not with altered endocervica

99 timing of NLRP3 expression and production of inflammatory cytokines by macrophages.

100 Synthesis of inflammatory cytokines by monocytes, alone or in the pre

101 ress, IKK/NF-kappaB and JNK/AP-1 activation, inflammatory cytokine, chemokine, and adhesion molecule

102 roved renal function due to diminished local inflammatory cytokine/chemokine levels and neutrophil re

103 Increases in mRNA level or stability of pro-inflammatory cytokines/chemokines are abolished by PARP1

104 ant differences in their plasma levels of 38 inflammatory cytokines/chemokines measured using multipl

105 C-NPC co-culture, ConA-induced expression of inflammatory cytokines/chemokines was significantly augm

106 sion of adhesion molecules and pro- and anti-inflammatory cytokines/chemokines, microglial activation

107 hich manifested as an increase in plasma pro-inflammatory cytokines compared to control mice.

108 H3K4me3 at inflammatory gene promoters, and inflammatory cytokines compared with controls.

109 nd ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts.

110 occupy key cellular niches and elaborate pro-inflammatory cytokines, contributing to aging-related di

111 ands in challenging environments, as well as inflammatory cytokine-driven target genes.

112 Further analyses of changes in levels of inflammatory cytokines during DAA treatment also provide

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

114 Mice lacking GAS6 presented higher levels of inflammatory cytokines, elevated frequencies of neutroph

115 ce, which was accompanied by tumor-promoting inflammatory cytokine expression and acquisition of the

116 osure to the host immune system, diminishing inflammatory cytokine expression and promoting intramacr

117 ar suppressive effect on TLR-stimulation and inflammatory cytokine expression from macrophages than t

118 nstrate that PDE4B negatively modulates anti-inflammatory cytokine expression in innate immune cells,

119 ith Myr significantly decreased AGEs-induced inflammatory cytokine expression, limited an increase in

120 antly reduced in vivo lung pathology and pro-inflammatory cytokine expression.

121 atory cytokines and higher secretion of anti-inflammatory cytokines from activated cardiac MSCs of TL

122 y secretion of both proinflammatory and anti-inflammatory cytokines from murine mDCs and PBMCs from p

123 ulates Th1 differentiation, secretion of the inflammatory cytokine gamma interferon (IFN-gamma), and

124 ikely an effect of the overproduction of pro-inflammatory cytokines generated in MAVS-deficient mice

125 gy, carbohydrate analysis, and expression of inflammatory cytokine genes.

126 riming and elevated T cell expression of the inflammatory cytokine GM-CSF, concomitant with pancreati

127 microglial activation and the production of inflammatory cytokines, highlighting the role of inflamm

128 ro, exposure of proximal tubule cells to the inflammatory cytokines IFN-gamma and TNF-alpha led to in

129 Treatment of HDLECs with the pro-inflammatory cytokines IFN-gamma and TNF-alpha synergist

130 bserved increased gene expression of the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-1beta an

131 Here, we show that ablation of the anti-inflammatory cytokine IL-10 improves insulin sensitivity

132 In this study, we demonstrated that anti-inflammatory cytokine IL-10 was a critical mediator for

133 ung damage, increased production of the anti-inflammatory cytokine IL-10, and vastly improved mouse s

134 enhancing the release of the regulatory/anti-inflammatory cytokine IL-10.

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

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

137 o seizures and have high brain levels of the inflammatory cytokine IL-1beta.

138 eceptor 2 and induces the release of the pro-inflammatory cytokine IL-6 from cells.

139 found to secrete greater amounts of the pro-inflammatory cytokine IL-6, compared to those from norma

140 tivation of caspase-1 and the release of pro-inflammatory cytokines IL-1beta and IL-18 accompanied by

141 upture of the cell causes release of the pro-inflammatory cytokines IL-1beta and IL-18, alarmins and

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

143 s the repression of NF-kappaB, EDN-1 and pro-inflammatory cytokines IL-6, IL-12, and TNFalpha.

144 c inflammation with later local increases in inflammatory cytokine (IL-17) production, which could ha

145 Th2 cytokines (IL-4, IL-5 & IL-13) and anti-inflammatory cytokines (IL-10) in the bronchoalveolar fl

146 sia (Ki67) and in the dermal infiltration of inflammatory cytokines (IL36alpha, pSTAT3, TNFalpha, NFk

147 Levels of inflammatory cytokines (IL6) and chemokines were signifi

148 is and their colonic tissues did not produce inflammatory cytokines (IL6, IL9, or IL13).

149 athways linked to smooth muscle contraction, inflammatory cytokines, immune mediators, extracellular

150 on and functional transition from cytotoxic, inflammatory cytokine immunity, to cell expansion with d

151 Validation studies confirmed inflammatory cytokine impairment of BM that could be rev

152 IL-17 is a pro-inflammatory cytokine implicated a variety of autoimmune

153 plicate a potential therapeutic role of anti-inflammatory cytokine in the treatment of aging-mediated

154 ent was demonstrated by reduced secretion of inflammatory cytokines in affected skin tissue from NC/N

155 inding to and activation of the promoters of inflammatory cytokines in human monocytes.

156 clear translocation of IRF5 and induction of inflammatory cytokines in human monocytes.

157 horylation, the ISR and the induction of pro-inflammatory cytokines in human THP1 macrophages submitt

158 nts with UC and correlate with production of inflammatory cytokines in mice and humans.

159 imilarly, luteolin inhibits induction of pro-inflammatory cytokines in murine microglial macrophages.

160 ial cells, HRVs induce the production of pro-inflammatory cytokines in PBMCs.

161 viously shown to display increased levels of inflammatory cytokines in peripheral and central tissues

162 additionally, B cells produce pro- and anti-inflammatory cytokines in response to certain stimuli.

163 sa expresses protective interferon (IFN) and inflammatory cytokines in response to respiratory syncyt

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

165 ines, which are believed to function as anti-inflammatory cytokines in T1D.

166 The levels of inflammatory cytokines in the serum (TNF-alpha, IL-6, IL

167 tory cell infiltration and the production of inflammatory cytokines in the skin.

168 ti-inflammatory cytokines and reduced in pro-inflammatory cytokines in treated mice.

169 Gene expression analysis revealed that anti-inflammatory cytokines including IL-10 and IL-11 as well

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

171 Gemcitabine increased inflammatory cytokines including TIMP1 in the KPC mouse

172 exposure also increased expression of major inflammatory cytokines, including chemotactic factors.

173 ation play a role in potentiating PH and pro-inflammatory cytokines, including TNF, are associated wi

174 sociated with elevated levels of circulating inflammatory cytokines, including TNF-alpha, IFN-gamma,

175 has been associated with increased levels of inflammatory cytokines, including tumor necrosis factor

176 ole in the elevations in cutaneous and serum inflammatory cytokines induced by epidermal dysfunction.

177 This related to inflammatory cytokine induction by SVLP(+) DCs, with ada

178 articles with strong interferon and mild pro-inflammatory cytokine induction may qualify as vaccine a

179 xample increasing the expression of the anti-inflammatory cytokine interleukin 10 (IL-10), and decrea

180 to inhibit the expression of the potent anti-inflammatory cytokine interleukin 10 (IL-10).

181 K1 and -2 promote the expression of the anti-inflammatory cytokine interleukin 10, it did not strongl

182 e here that PDE4 inhibitors enhance the anti-inflammatory cytokine interleukin-1 receptor antagonist

183 ith increased circulating levels of the anti-inflammatory cytokine interleukin-10 (IL-10).

184 increases microglial expression of the anti-inflammatory cytokine interleukin-10 (IL-10).

185 xpression, while monocytes expressed the pro-inflammatory cytokine interleukin-1beta (IL-1beta).

186 -1 function also inhibits release of the pro-inflammatory cytokine interleukin-1beta from activated m

187 loss of SGNs and enhanced expression of the inflammatory cytokine interleukin-1beta, when compared t

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

189 fficking steps underlying the release of the inflammatory cytokine interleukin-6 (IL-6) from human bl

190 KO mice show increased expression of the pro-inflammatory cytokine interleukin-6 (IL-6) relative to B

191 Increased c-Fos induced inflammatory cytokines interleukin 6 (IL-6) and tumor ne

192 pathway leading to the generation of the pro-inflammatory cytokines interleukin-1beta and interleukin

193 s; levels of GATA3 correlated with levels of inflammatory cytokines (interleukin [IL] 9, IL17A, IL6,

194 The inflammatory cytokine, interleukin-6 (IL-6), is a critic

195 mune responses by facilitating maturation of inflammatory cytokines, interleukin (IL)-1beta and IL-18

196 Production of pro-inflammatory cytokines is reduced by ex vivo gene-silenc

197 ivity regulates the production of downstream inflammatory cytokines is unclear.

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

199 ificant decreases in both local and systemic inflammatory cytokine levels and in fibrosis, suggesting

200 In addition, MyD88(-/-) joint inflammatory cytokine levels on day 3 and beyond were si

201 The inflammatory cytokine levels were much lower in IFOT tha

202 epharitis, meibomian gland capping) and tear inflammatory cytokine levels.

203 The anti-inflammatory cytokine M-CSF, but not DC growth factors,

204 therapies modulating vasoactive mediators or inflammatory cytokines may not affect ME in ERM patients

205 expand during states of elevated circulating inflammatory cytokines, may link the systemic inflammati

206 helial corneal integrity, and reduce the pro-inflammatory cytokine milieu in the tissue.

207 Inflammatory cytokines modify the tumour microenvironmen

208 TGF-beta1 also increased levels of inflammatory cytokine monocyte chemoattractant protein-1

209 t the OSPW-OF had significant effects on pro-inflammatory cytokine mRNA levels and cytokine protein s

210 IL-37, a newly found anti-inflammatory cytokine of the IL-1 family, has both extra

211 imicrobial effector responses, which include inflammatory cytokine or interferon expression, downregu

212 ls, DAC enhanced messenger RNA expression of inflammatory cytokines, perforin, and TRAIL by HSPC-NK c

213 protease caspase-1, which activates the pro-inflammatory cytokine precursors pro-IL-1beta and pro-IL

214 s of immune cells and elevated levels of pro-inflammatory cytokines predict poor prognosis.

215 kine-producing and lower frequencies of anti-inflammatory cytokine-producing dendritic cells (DCs) an

216 s from rheumatoid arthritis patients reduced inflammatory cytokine production and increased IL-10 pro

217 cells require sustained Ca(2+) signaling for inflammatory cytokine production and the killing of targ

218 ate, colonic infiltration of neutrophils and inflammatory cytokine production are impaired in M-ILK-d

219 responses and that tumor-induced central pro-inflammatory cytokine production can exist in the absenc

220 Interpretation: Pro-inflammatory cytokine production had a dose-dependent an

221 ion of CD4(+) and CD8(+) cells and inhibited inflammatory cytokine production in a manner that was ab

222 (LPS) induces both pro-inflammatory and anti-inflammatory cytokine production in macrophages.

223 ted with decreased microglial activation and inflammatory cytokine production in the retina in vivo a

224 nfection with wild-type S. aureus suppressed inflammatory cytokine production in the skin of female,

225 wever, this can be reversed by inhibition of inflammatory cytokine production that can be used to pro

226 Higher Vdelta2 pro-inflammatory cytokine production was associated with pro

227 ate GSH levels and attenuate LPS-induced pro-inflammatory cytokine production was inhibited by buthio

228 st that peripheral tumors elicit central pro-inflammatory cytokine production, in turn leading to dep

229 LipA-deficient strain induces heightened pro-inflammatory cytokine production, which is diminished in

230 nonuclear cell infiltrate and high levels of inflammatory cytokine production.

231 g antimicrobial pathways while also limiting inflammatory cytokine production.

232 luid loss into the intestine, and increasing inflammatory cytokine production.

233 isease progression such as VIC activation or inflammatory cytokine production.

234 ciated with diminished Vdelta2(+) T cell pro-inflammatory cytokine production.

235 athological neutrophil phenotype and an anti-inflammatory cytokine profile associated with heightened

236 otype and an increased anti-inflammatory/pro-inflammatory cytokine ratio.

237 rough Toll-like receptor 9 (TLR9) along with inflammatory cytokine receptor IFN-gamma receptor (IFN-g

238 in a marked reduction in the serum levels of inflammatory cytokines, reduced disease burden, and reve

239 S treated mice were accompanied by increased inflammatory cytokines, reduced mucin production and dys

240 ed with decreased serum concentration of pro-inflammatory cytokines, reduced neutrophil infiltration

241 n in vivo accompanied by markedly attenuated inflammatory cytokine release in response to LPS.

242 A that was associated with a more pronounced inflammatory cytokine response.

243 Despite having significantly reduced inflammatory cytokine responses to LPS and bacterial inf

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

245 re of HAECs to oxidized phospholipids or pro-inflammatory cytokines results in signal-specific altera

246 sferase levels, apoptotic markers, and human inflammatory cytokines returned to pretreatment levels w

247 AMA0825 did not affect pro-inflammatory cytokine secretion from other ROCK-positive

248 Despite the absence of inflammatory cytokine secretion, mDCs incubated with P.

249 1.69, 1.71 and 1.63), and a pro- to an anti-inflammatory cytokine shift.

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

251 These findings provide evidence that inflammatory cytokine signaling is a key process underly

252 key mediator of toll-like receptors and pro-inflammatory cytokine signaling pathways.

253 or miR-718 in controlling TLR4 signaling and inflammatory cytokine signaling through a negative feedb

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

255 riven by growth factors such as VEGF and pro-inflammatory cytokines such as TNF-alpha.

256 sion molecules and chemokines induced by pro-inflammatory cytokines such as TNFalpha and IFNgamma, bu

257 losartan may differently control balance of inflammatory cytokines, such as IL-6 and IL-8, in primar

258 but resulted in attenuated induction of anti-inflammatory cytokines, such as interleukin (IL)-10 and

259 V infection, especially during the post-cART inflammatory cytokine surge, likely limit cellular respo

260 Levels of anti-inflammatory cytokine TGF-beta remained practically unaf

261 ory proinflammatory cytokines and lower anti-inflammatory cytokines than Cd36(-/-) mice.

262 lower metabolic activity and release of pro-inflammatory cytokines than CFC tissue, but surprisingly

263 e we show that Prostaglandin E2 (PGE2) is an inflammatory cytokine that directly targets MuSCs via th

264 Interleukin 10 (IL-10) is an anti-inflammatory cytokine that plays a critical role in the

265 TNF is an inflammatory cytokine that upon binding to its receptor,

266 n-1alpha (IL-1alpha) and IL-1beta are potent inflammatory cytokines that activate local and systemic

267 ukin-27 (IL-27) and IL-37 are two known anti-inflammatory cytokines that are highly expressed in S. s

268 receptor (AT1R) contributes to production of inflammatory cytokines that are important for periodonta

269 In animal studies, central and blood borne inflammatory cytokines that can be elevated in RA evoke

270 IL-4 and IL-13 have been defined as anti-inflammatory cytokines that can counter myelin-reactive

271 hile the array data did implicate a group of inflammatory cytokines that were elevated in a subset of

272 ctivates DDR and increases the expression of inflammatory cytokines through NF-kappaB signalling.

273 g functional recovery after SCI by dampening inflammatory cytokines, thus pointing towards a new dire

274 rget of Mi-2beta in keratinocytes is the pro-inflammatory cytokine thymic stromal lymphopoietin (TSLP

275 MDM showed ImI-mediated upregulation of pro-inflammatory cytokine TNF-alpha in an ImI concentration-

276 migration in the absence and presence of an inflammatory cytokine (TNF-alpha) and a well-known cell

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

278 tease, responsible for the liberation of the inflammatory cytokine TNFalpha and ligands of the epider

279 The inflammatory cytokine TNFalpha causes EC apoptosis while

280 ence of network perturbations induced by the inflammatory cytokines TNFalpha, IL1beta, and IFNgamma.

281 kers of inflammation (C-reactive protein and inflammatory cytokines) to assess the influence of these

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

283 Plasma levels of the inflammatory cytokine tumor necrosis factor alpha (TNFal

284 r atrophy was associated with high levels of inflammatory cytokines: tumor necrosis factor, interleuk

285 ions by releasing cytotoxic granules and pro-inflammatory cytokines upon recognition of diseased cell

286 ortantly, strongly reduced the production of inflammatory cytokines upon stimulation with aminobispho

287 oorly with WT Tregs in vivo and produced pro-inflammatory cytokines upon stimulation.

288 PE explants activated the production of anti-inflammatory cytokines via an aryl hydrocarbon receptor

289 ing an array assessing the expression of 102 inflammatory cytokines we similarly did not observe a ma

290 plasma, high levels of human T helper 2-type inflammatory cytokines were detectable, which activated

291 Results show pro-inflammatory cytokines were down-regulated significantly

292 Eight proinflammatory and anti-inflammatory cytokines were measured on acute respirator

293 gh mobility group box 1 (HMGB1) serves as an inflammatory cytokine when secreted extracellularly in p

294 Interleukin-17 (IL-17) is a critical pro-inflammatory cytokine, which has been demonstrated to pr

295 h MSC-Ex completely blocked the induction of inflammatory cytokines, which were strongly detected in

296 TGF-beta is an anti-inflammatory cytokine whose signaling is negatively cont

297 acrophages from Cmah(-/-) mice secreted more inflammatory cytokines with LPS stimulation and showed m

298 nd smooth muscle cells were treated with pro-inflammatory cytokines with or without aldosterone, nucl

299 wn of Irf5 blunted CB1R-induced secretion of inflammatory cytokines without affecting CCL2 expression

300 ed that patients with elevated pro- and anti-inflammatory cytokines would have higher mortality rates