ライフサイエンスコーパス: inflammatory cytokine

1 -like microglia and increased release of pro-inflammatory cytokines.

2 ough changes in genital tract microbiota and inflammatory cytokines.

3 n, foam cell formation and expression of pro-inflammatory cytokines.

4 necrosis factor-alpha (TNF-alpha) and other inflammatory cytokines.

5 M1, since they did not produce pro- and anti-inflammatory cytokines.

6 by immune cells and increased expression of inflammatory cytokines.

7 gut and skin are treated with inhibitors of inflammatory cytokines.

8 gut contains innate lymphoid cells producing inflammatory cytokines.

9 cells reduce tumour growth and express more inflammatory cytokines.

10 piratory burst, phagocytosis, and release of inflammatory cytokines.

11 ons which may be controlling the response to inflammatory cytokines.

12 mortality due to sustained production of pro-inflammatory cytokines.

13 ith putative markers of disease severity and inflammatory cytokines.

14 and crucially, a range of anti-viral and pro-inflammatory cytokines.

15 C-iTregs) are stable, even after exposure to inflammatory cytokines.

16 is associated with the production of various inflammatory cytokines.

17 diseases by mediating the expression of pro-inflammatory cytokines.

18 main-binding motif in the promoter region of inflammatory cytokines.

19 , children generally produce lower levels of inflammatory cytokines.

20 and sputum, blood leucocyte counts and serum inflammatory cytokines.

21 independent TLRs to produce higher levels of inflammatory cytokines.

22 omote responsiveness to oxidative stress and inflammatory cytokines.

23 osed to LPS as well as other TLR ligands and inflammatory cytokines.

24 e, we used a hemoadsorber (HA) to remove pro-inflammatory cytokines.

25 es do not express substantial amounts of pro-inflammatory cytokines.

26 s in vivo and reduced systemic levels of pro-inflammatory cytokines.

27 degranulation response but robustly produce inflammatory cytokines.

28 r cells to gp96 induced the secretion of pro-inflammatory cytokines.

29 ing Ly6C(+) monocytes and macrophage-derived inflammatory cytokines.

30 -treated RMs, paralleled by increases in the inflammatory cytokines.

31 activity, including increased levels of pro-inflammatory cytokines(3,4) that may be produced by a su

32 s beneficial, abolishing production of a key inflammatory cytokine, accelerating weight regain, and l

33 anistically, inhibition of miR-15a increases inflammatory cytokines, activates caspase-1 inflammasome

34 Oxidative stress and inflammatory cytokines affect the human brain, increasin

35 ammatory signature, including high levels of inflammatory cytokines, alveolar inflammatory infiltrate

36 demonstrates that over-expression of an anti-inflammatory cytokine and a decoy chemokine receptor can

37 It serves as an inflammatory cytokine and chemokine, but also exhibits e

38 IL-35 is an anti-inflammatory cytokine and is thought to be produced by r

39 characterized by excessive production of pro-inflammatory cytokines and acute lung damage associated

40 s increased levels of KLF2, produce less pro-inflammatory cytokines and adhesion molecules.

41 nflammatory cells, and the production of pro-inflammatory cytokines and adhesion molecules.

42 a significant reduction in the levels of pro-inflammatory cytokines and an increase in IgA levels and

43 els (n=30), and plasma samples for levels of inflammatory cytokines and chemokines (n=81).

44 ly genes (for example, Egr1, Fos, Dusp1) and inflammatory cytokines and chemokines (tumour necrosis f

45 ion of Th17/Th1 cell subsets with release of inflammatory cytokines and chemokines and accumulation o

46 ry signalling pathways and overproduction of inflammatory cytokines and chemokines compared with unaf

47 paralleled by elevated levels of several pro-inflammatory cytokines and chemokines in ascites fluid a

48 ein analysis showed differential profiles of inflammatory cytokines and chemokines in the UCL and NUC

49 S activated mRNA expression of different pro-inflammatory cytokines and chemokines in time- and conce

50 Inflammatory cytokines and chemokines were examined in t

51 ent of CD8(+) T cells, reduced production of inflammatory cytokines and chemokines, and no delay in t

52 PG-CAT greatly reduced the concentration of inflammatory cytokines and chemokines, including IL-1, T

53 egulated and modulated the expression of pro-inflammatory cytokines and chemokines.

54 been found to restrain rather than activate inflammatory cytokines and immune signaling.

55 ion, literature characterizing the milieu of inflammatory cytokines and lipid mediators in AERD has b

56 tion was associated with increased levels of inflammatory cytokines and macrophage activation.

57 Elevated local production of inflammatory cytokines and MMPs, together with apparent

58 Increased production of inflammatory cytokines and myeloid-derived suppressor ce

59 otentiate neuronal activity by releasing pro-inflammatory cytokines and neuroactive compounds.

60 iRNA interactome controlling the response to inflammatory cytokines and novel mediators of inflammati

61 long a continuum from reliance on innate pro-inflammatory cytokines and stress-induced host ligands t

62 ve agents in soy and tomatoes can reduce pro-inflammatory cytokines and suppressive immune population

63 sponses are potentially counteracted by anti-inflammatory cytokines and type 2 responses.

64 factors (for example, insulin, oestrogen and inflammatory cytokines) and their intracellular pathways

65 the blood-brain barrier (BBB), formation of inflammatory cytokines, and brain infiltration of blood-

66 lammation (increased leukocyte infiltration, inflammatory cytokines, and chemokines), oxidative stres

67 retinoic acid, dampen their capacity to make inflammatory cytokines, and increase their responsivenes

68 s intrauterine UP infection, upregulates pro-inflammatory cytokines, and increases preterm birth rate

69 of cysteine protease caspase-1, secretion of inflammatory cytokines, and induction of inflammatory ce

70 V strain induced IFN-stimulated transcripts, inflammatory cytokines, and intestinal expression of STA

71 in levels, BAL inflammatory cell counts, pro-inflammatory cytokines, and pulmonary function (total lu

72 phocytes, decreased inhibitory and increased inflammatory cytokines, and reduced angiogenesis and met

73 mediated by oxidative stress, DNA damage, or inflammatory cytokines, and these factors may act synerg

74 While multiple inflammatory cytokines are produced by innate immune cel

75 Inflammatory cytokines are sufficient for memory CD8 T c

76 eneity and examine the potentiality of using inflammatory cytokines as novel predictive markers for t

77 l and dynamic responses of genes to specific inflammatory cytokines as well as miRNAs that are differ

78 y reduce AVI, with more durable reduction in inflammatory cytokines associated with cardiovascular di

79 These results show that inflammatory cytokines associated with HIV-1 infection i

80 of psoriasis by regulating the expression of inflammatory cytokines associated with macrophage activa

81 r-associated fibroblasts (CAFs) that express inflammatory cytokines at high levels.

82 barriers to care and showed increased serum inflammatory cytokines but did not show differences in a

83 oV-2 can lead to excessive production of pro-inflammatory cytokines, but the production of type I int

84 or virulence and did not induce secretion of inflammatory cytokines by epithelial cells.

85 xes, Fc afucosylation enhanced production of inflammatory cytokines by monocytes, including interleuk

86 paB, which, in turn, elevated the release of inflammatory cytokines by the tumor cells.

87 IL-10 is a potent anti-inflammatory cytokine capable of suppressing a number of

88 Inflammatory cytokine/chemokine concentrations were dete

89 XAA in MCC cells reactivates their antitumor inflammatory cytokine/chemokine production.

90 Inflammatory cytokines, chemokines and bone markers were

91 ion in target organs, systemic production of inflammatory cytokines, chemokines and specific humoral

92 Fiber reduced expression of genes encoding inflammatory cytokines, chemokines, and fibrosis-promoti

93 pid A (DPLA), and parameters of fibrosis and inflammatory cytokines/chemokines were determined by qRT

94 eater potency and reduced systemic levels of inflammatory cytokines compared to CAR T cells administe

95 Cervicovaginal inflammatory cytokine concentrations were significantly

96 s, including T-regulatory cells that produce inflammatory cytokines; CXCR3+ plasmablasts; and IL1B+ m

97 f RNA-sequencing data reveals that genes for inflammatory cytokines/cytokine receptors are significan

98 s-in particular the ECM protease ADAMTS4-and inflammatory cytokines, damage-responsive fibroblasts mo

99 ll transplant is an allo-reactive T cell and inflammatory cytokine driven organ injury with epithelia

100 In response to secretion of inflammatory cytokines (e.g., IL1B) from immune infiltra

101 d increased microbial translocation, we find inflammatory cytokines (e.g., interferon gamma [IFN-gamm

102 now termed miR-147), a negative regulator of inflammatory cytokines (e.g., interleukin-6 [IL-6] and I

103 y a critical role in immunity by shaping the inflammatory cytokine environment in a variety of physio

104 Elevated pro-inflammatory cytokines exist in both blood and brain of

105 y were used to determine the presence of pro-inflammatory cytokine expressing monocytes and monocyte-

106 ty, delayed cellular senescence, and reduced inflammatory cytokine expression and changes in VSMC met

107 an innate sensor of DENV particles inducing inflammatory cytokine expression and impairing vascular

108 Microglial morphology and inflammatory cytokine expression were analysed by immuno

109 phage infiltration, proinflammatory and anti-inflammatory cytokine expression, and fibrosis along the

110 ion, prevents Toll-like receptor-induced pro-inflammatory cytokine expression, and represents an effe

111 and macrophage content, plaque size, and pro-inflammatory cytokine expression.

112 on in the injured brain areas by suppressing inflammatory cytokines expression whereas free Sino trea

113 of Interleukin-10 (IL-10), a classical anti-inflammatory cytokine, extends lifespan in the SOD1-G93A

114 is characterized by the rapid production of inflammatory cytokines following delivery of therapy, wi

115 increase in the levels of immune stimulatory inflammatory cytokines, for example, IFN-gamma and IL-12

116 In a separate mouse cohort, pro-inflammatory cytokine gene expression and 1H nuclear mag

117 d adipose tissue macrophage infiltration and inflammatory cytokine gene expression.

118 ted the cGAS/STING/IRF3 pathway, stimulating inflammatory cytokine generation.

119 ne suppressed the cPAF-induced expression of inflammatory cytokine genes Il1b, Il6, and Il10 in the d

120 steogenic genes, decreased expression of pro-inflammatory cytokine genes, and increased abundance of

121 nted on MHC Ag alone, we show that different inflammatory cytokines have comparable Ag dose threshold

122 Surprisingly, the anti-inflammatory cytokine IL-10, but not the pro-inflammator

123 uity pathway analyses also suggested the pro-inflammatory cytokine IL-17A to regulate the vaginal hos

124 , resident islet macrophages release the pro-inflammatory cytokine IL-1beta, to levels that are suffi

125 iated with an elevation in the levels of the inflammatory cytokine IL-6 in the aorta, which participa

126 caused by chronic overexpression of the pro-inflammatory cytokine IL-6.

127 IL-12, (ii) an increase in the level of the inflammatory cytokine IL-6; and (iii) downregulation of

128 riaxone in reducing the secretion of the pro-inflammatory cytokine IL-8 by endocervical cells infecte

129 From a panel of 10 cytokines, the pro-inflammatory cytokine IL-8 exhibited a strong correlatio

130 iling hMSCs exhibited increased secretion of inflammatory cytokines IL (interleukin)-1beta (98%, P<0.

131 three days of treatment was detected for pro-inflammatory cytokines IL-1beta, IL-2, IL-6, IL-8 and TN

132 lpha, IFN-gamma, and IL-2 more than the anti-inflammatory cytokines IL-4 and IL-10 in tonsil and bloo

133 inflammatory cytokine IL-10, but not the pro-inflammatory cytokines IL-6 or IL-21, is required via ST

134 argely not affected by STEMI, except for pro-inflammatory cytokines IL-6, IL-18, and MIG, as well as

135 very early (6 and 12 h) 12/15-LOX-dependent inflammatory cytokine (IL-1alpha, IL-1beta, and TNF-alph

136 followed by the expression and secretion of inflammatory cytokines (IL [interleukin] 1B, IL6, and TN

137 ratinocyte proliferation (Ki67+, KRT16), and inflammatory cytokines (IL-17A/C/F, IL-23A, IL-12B) decr

138 ease relative to control, P<0.01) and plasma inflammatory cytokines (IL-1alpha [interleukin 1alpha],

139 enuation of aortic diameter, decrease in pro-inflammatory cytokines (IL-1beta, IL-6, IL-17, MCP-1, MI

140 or antagonists (IL-1Ra, IL-36Ra), and 2 anti-inflammatory cytokines (IL-37, IL-38).

141 in vitro and in vivo, the expression of pro-inflammatory cytokines (IL-6, IL-1beta, and TNF-alpha) w

142 reased indistinctively the production of pro-inflammatory cytokines (IL-8, IL-1beta, and IL-6).

143 glia, along with elevated levels of the anti-inflammatory cytokine, IL-10 were observed in the hippoc

144 is sufficient for the expression of the anti-inflammatory cytokine, IL-10, in T(H)17 cells.

145 receptors, T regulatory cells, and the anti-inflammatory cytokine, IL-10, that antagonizes both inna

146 of NFkappaB signaling, increase of the anti-inflammatory cytokines IL10 and IL12P40, and increased e

147 lation between MARCO expression and the anti-inflammatory cytokine IL37.

148 al mediator is interleukin-17 (IL-17), a pro-inflammatory cytokine implicated in neurodevelopmental d

149 volumes, as shown for the detection of a pro-inflammatory cytokine in mouse interstitial fluid and of

150 em to skew toward M1 macrophages and release inflammatory cytokines in an MyD88-dependent manner, wit

151 ts of perioperative intravenous n-3 PUFAs on inflammatory cytokines in colon cancer surgery.

152 vermectin induced NLRP3 inflammasome and pro-inflammatory cytokines in cultured human proximal tubule

153 86S mutant) leads to increased expression of inflammatory cytokines in infected Caco-2 cells.

154 between gut microbiota changes and increased inflammatory cytokines in insomnia patients.

155 p38 MAPK-, and JNK-dependent and evoked anti-inflammatory cytokines in macrophage cocultures.

156 amily, regulates the sustained production of inflammatory cytokines in macrophages triggered by TLR s

157 ction in RM and underscore the importance of inflammatory cytokines in mucosal HIV infection, demonst

158 DCA can attenuate the provoked expression of inflammatory cytokines in oral fibroblasts, oral human s

159 d B cells activity and the production of pro-inflammatory cytokines in P. gingivalis-stimulated innat

160 li reduced the production of the majority of inflammatory cytokines in response to G. vaginalis, isol

161 lved in pyroptotic cell death and release of inflammatory cytokines in response to pathogen patterns

162 /-) mice significantly reduced production of inflammatory cytokines in response to the GCP-rCpa1 vacc

163 ed weight loss, macrophage infiltration, and inflammatory cytokines in the colon tissue.

164 late STAT3, and failed to reduce LPS induced inflammatory cytokines in the presence of exogenous IL-1

165 mic analyses revealed significantly elevated inflammatory cytokines in the supernatants of the GL261

166 ter acute lung injury (ALI) express more pro-inflammatory cytokines in their brainstem respiratory co

167 psoriasis while also lowering levels of pro-inflammatory cytokines in tissue and serum.

168 gmented expression of IL-10, a critical anti-inflammatory cytokine, in turn, attenuated production of

169 ed atherosclerosis reduced the production of inflammatory cytokines including IL (interleukin)-1beta

170 regulatory B cells (Bregs) that produce anti-inflammatory cytokines including interleukin 10 (IL-10),

171 nscriptome, suppressed the production of pro-inflammatory cytokines (including interleukin-6, tumor n

172 yed elevated peripheral production of innate inflammatory cytokines, including IL-1beta, IL-6, and TN

173 Inflammatory cytokines induce the expression of IFITM3 i

174 The pattern of pro-inflammatory cytokines induced in COVID-19 has similarit

175 Tregs suppress effector T cell-mediated and inflammatory cytokine-induced CEnC death, and to elucida

176 estin, Sox2, and PAX6), reduction of the pro-inflammatory cytokines INFG, IL1A, and IL12P70 through t

177 apacity and suppressed the expression of pro-inflammatory cytokines, iNOS, IL6, and IL1beta, compared

178 ocytes that increased production of systemic inflammatory cytokines instead of accumulating lipids, w

179 rating cell nuclear antigen (PCNA), the anti-inflammatory cytokine interleukin (IL) 10, and the apopt

180 s that are the main local source of the anti-inflammatory cytokine interleukin-10 (IL-10) and the met

181 vealed increased immunoreactivity of the pro-inflammatory cytokine Interleukin-1beta (IL-1beta) in th

182 to trigger the maturation and release of the inflammatory cytokine interleukin-1beta (IL-1beta).

183 cell deficiency, had increased levels of the inflammatory cytokine interleukin-6 (IL-6) and decreased

184 It also prevented induction of inflammatory cytokines interleukin-6 and osteopontin, lo

185 among plasma and CSF CRP and plasma and CSF inflammatory cytokines (interleukin [IL]-6, tumor necros

186 The anti-inflammatory cytokines (interleukin-4 [IL-4], IL-6, and

187 AF patients have elevated levels of inflammatory cytokines known to promote vascular leak, s

188 ood of patients with PTA showed a higher pro-inflammatory cytokine level compared to the samples of p

189 colon injury, with a concomitant increase in inflammatory cytokine levels and oxidative and DNA damag

190 Increased pro-inflammatory cytokine levels and proliferation of activa

191 at maternal immune activation (MIA) elevates inflammatory cytokine levels in the maternal and fetal c

192 Inflammatory cytokine levels, presence, and quantities o

193 jection of the hybrid system locally reduces inflammatory cytokine levels.

194 We measured inflammatory cytokine levels.

195 are enhanced, leading to a reduction in pro-inflammatory cytokine levels.

196 vided blood samples that were used to assess inflammatory cytokines levels.

197 involved in the regulation of antioxidants, inflammatory cytokines, lipid metabolism, and organ grow

198 p63-mediated activation of enhancers at pro-inflammatory cytokine loci, which includes IL1A and CXCL

199 h autism and intellectual disability; (2) an inflammatory cytokine mixture (ICM) comprised of five cy

200 ognised important in pain regulation through inflammatory cytokine modulation of peripheral nocicepti

201 ace charges displayed on the majority of pro-inflammatory cytokines (negative) and anti-inflammatory

202 els of HF, central inhibition of RAS and pro-inflammatory cytokines normalizes sympathetic drive and

203 nd decreases the expression of important pro-inflammatory cytokines of Th1 and Th17 profiles, while i

204 types, cognate innate immune receptors, and inflammatory cytokines on parasite control and disease s

205 prolonging antimicrobials, direct effects of inflammatory cytokines on ventricular repolarization are

206 ated with elevated circulating levels of pro-inflammatory cytokines opened a new area of research tha

207 is, macrophages and monocytes are exposed to inflammatory cytokines, oxidized lipids, cholesterol cry

208 By investigating temporal IFN and inflammatory cytokine patterns in 32 moderate-to-severe

209 M-CSF), a myelopoietic growth factor and pro-inflammatory cytokine, plays a critical role in alveolar

210 o-inflammatory cytokines (negative) and anti-inflammatory cytokines (positive) allow for the selectiv

211 e of PMN to Mtb LAM did elicit pro- and anti-inflammatory cytokine production and release in a TLR2/1

212 itigates aortic smooth muscle cell-dependent inflammatory cytokine production as well as decreases ne

213 cts with elevated anticardiolipin stimulates inflammatory cytokine production by endothelial cells an

214 nd normalization of proinflammatory and anti-inflammatory cytokine production by macrophages.

215 IFN-beta did not induce inflammatory cytokine production by MDMs or PBECs but re

216 i) ZIKV RNA-positive monocytes and a lack of inflammatory cytokine production compared to mice inocul

217 us, IRF5 acts as a regulator of myeloid cell inflammatory cytokine production during IAV infection in

218 converts DAG into phosphatidic acid, limits inflammatory cytokine production in an arthritic mouse m

219 mpened pathology, leukocyte recruitment, and inflammatory cytokine production in lungs including TNF,

220 Intriguingly, GM-CSF signaling amplifies inflammatory cytokine production in recruited monocytes

221 DAG/phosphatidic acid axis as a modulator of inflammatory cytokine production in sJIA and CSS.

222 ent contributed directly to cytotoxicity and inflammatory cytokine production of bone marrow-derived

223 roduced less lactic acid and induced greater inflammatory cytokine production than those from women w

224 adipose tissue-mediated inflammation and pro-inflammatory cytokine production, a shift towards ketone

225 condition showed increased permeability, pro-inflammatory cytokine production, and increased oxidativ

226 und that rolipram inhibits organ damage, pro-inflammatory cytokine production, and intracellular migr

227 -inducing molecule retinoic acid, inhibiting inflammatory cytokine production, and making macrophages

228 d IAV-driven immune pathology and associated inflammatory cytokine production, specifically reducing

229 ges, corresponded with reduced virus-induced inflammatory cytokine production, with IRF5 acting downs

230 sults also show that rolipram increases anti-inflammatory cytokine production.

231 ADD/RIPK1-dependent NF-kappaB activation and inflammatory cytokine production.

232 cts LPS, but not monophosphoryl lipid A, pro-inflammatory cytokine production.

233 thological damage is largely attributable to inflammatory cytokine production.

234 itor, PP2 completely prevents NE-induced pro-inflammatory cytokine production.

235 induced by PM in human DCs and increases pro-inflammatory cytokine production.

236 he changes in gut microbiota composition and inflammatory cytokines production associated with acute

237 -PE and IFN-gamma on AML blasts generated an inflammatory cytokine profile and activated NK cells.

238 Pro-inflammatory cytokine profile and multiple markers of ox

239 sponses, and consequently with high pro/anti-inflammatory cytokine ratios.

240 s, we discovered that PGA-FLUO inhibited pro-inflammatory cytokine release, suggesting that polypepti

241 o activate the NF-kappaB pathway and promote inflammatory cytokine release.

242 ges induce an interleukin-1 (IL-1)-dependent inflammatory cytokine response by recruited monocytes an

243 emonstrate that IL-27 indirectly promotes an inflammatory cytokine response during neonatal sepsis by

244 evere disease through production of damaging inflammatory cytokines, resulting in systemic inflammati

245 ic T-cell proliferation (in models 1 and 2), inflammatory cytokine secretion (in models 1, 2, and 3),

246 Functional enrichment analysis revealed pro-inflammatory cytokine signaling pathways as dysregulated

247 CDK4 regulated prometastatic inflammatory cytokine signaling, whereas CDK6 mainly con

248 TAT proteins can regulate both pro- and anti-inflammatory cytokine signaling.

249 ablation of SHMT2 causes strong increases in inflammatory cytokine signatures associated with redox d

250 tor gating, whereas MIA offspring with a low inflammatory cytokine status did not.

251 ivation and production of type I IFN and pro-inflammatory cytokines stimulated by TLR7/9 ligands.

252 Pro-inflammatory cytokine stimulation increased the cell sur

253 Similarly, all of the inflammatory cytokines studied significantly decreased a

254 EMT may potentially be induced by inflammatory cytokines such as CXCL12.

255 Caspase-1 cleaves and activates the pro-inflammatory cytokines such as IL-1beta and IL-18 and a

256 Elevated inflammatory cytokines such as IL-1beta and IL-18 and co

257 i and the tubulointerstitium cause AMR while inflammatory cytokines such as TNFalpha trigger graft in

258 On the contrary, pro-inflammatory cytokines such as tumor necrosis factor (TN

259 e immune systems, with pivotal roles for pro-inflammatory cytokines such as tumour necrosis factor, I

260 Several inflammatory cytokines, such as CD31, BDNF, TFF3, Serpin

261 on has been established, the effects of anti-inflammatory cytokines, such as IL-10, in TB are less we

262 Inflammatory cytokines, such as interleukin (IL)-1beta,

263 s from patients with cirrhosis produced more inflammatory cytokines than LPMs from controls.

264 geneic T cells and secreted higher levels of inflammatory cytokines than their steady-state counterpa

265 TNF is a highly pro-inflammatory cytokine that contributes not only to the r

266 Interleukin 10 (IL-10) is an anti-inflammatory cytokine that may be protective against cor

267 of interferon beta (IFNbeta), which is a pro-inflammatory cytokine that plays a major role in APC rec

268 adipose tissue, resulting in release of pro-inflammatory cytokines that impair lipolysis suppression

269 These macrophages generate inflammatory cytokines that induce cancer cell LCN2 expr

270 uction of mRNA transcripts which encode anti-inflammatory cytokines that promote inflammation resolut

271 In parallel, HDAC3 suppresses expression of inflammatory cytokines through a Rela-dependent mechanis

272 rus 2, and blocked by antibodies against the inflammatory cytokine TNF-alpha.

273 Stimulation increased the pro-inflammatory cytokines TNF-alpha, IFN-gamma, and IL-2 mo

274 hepatic antioxidants (Cu/Zn-SOD and GPx-4), inflammatory cytokines (TNF-alpha and TGF-beta1), lipid

275 early/acute inflammation by suppressing pro-inflammatory cytokines (TNF-alpha, IL-1beta, CCL-3 and I

276 reductions in the chemokine Ccl2 and the pro-inflammatory cytokine Tnfalpha were observed at the prot

277 al data to inform the threshold level of the inflammatory cytokine TNFalpha which initiates tissue fa

278 oteinases (MMPs), increase expression of pro-inflammatory cytokines TNFalpha, IL-1beta, and IL-8, and

279 es chemotherapy-induced secretion of the pro-inflammatory cytokines TNFalpha, IL-1beta, and IL-8.

280 agocytosis and does not induce expression of inflammatory cytokines TNFalpha, IL-6, IL-8 or IFNbeta.

281 vated fibroblasts produce high levels of pro-inflammatory cytokines to promote metastatic cancer grow

282 g T. gondii infection a strong NF-kappaB and inflammatory cytokine transcriptional signature is overr

283 class II [MHC-II], CD80, and CD86) and anti-inflammatory cytokine (transforming growth factor beta1

284 Notably, both visceral fat and the pro-inflammatory cytokine tumor necrosis factor alpha correl

285 CD163 can also bind to the pro-inflammatory cytokine TWEAK.

286 The expression of inflammatory cytokines was measured by reverse transcrip

287 Production of inflammatory cytokines was measured using MSD.Measuremen

288 Higher secretion of pro-inflammatory cytokines was seen in colonoids infected wi

289 Different intestinal inflammatory cytokines were also suppressed by homologou

290 The profiles of 16 major pro- and anti-inflammatory cytokines were analyzed in corneal lysates

291 dependently of disease severity, whereas pro-inflammatory cytokines were only acutely produced.

292 with MMP-9 activation and the production of inflammatory cytokines were resistant to pioglitazone.

293 nto the CNS, TLR7 enhances the production of inflammatory cytokines which contribute to immunopatholo

294 Sensing of inflammatory cytokines, which also include TNFalpha, is

295 the hypothalamic-pituitary-adrenal axis and inflammatory cytokines, which may contribute to disease

296 hat CTB EVs enhance decidual cell release of inflammatory cytokines, which we theorize is an importan

297 IL26 enhanced mouse-derived DNA induction of inflammatory cytokines, which were collectively importan

298 Interleukin-17A (IL-17A) is a pro-inflammatory cytokine with well-characterized biological

299 The coexpression of inflammatory cytokines with IL-22 is linked to the abili

300 Overall, the association of mostly anti-inflammatory cytokines with less tau pathology suggests