ライフサイエンスコーパス: proinflammatory cytokine

1 evels of reactive oxygen species and secrete proinflammatory cytokines.

2 P (YAP5SA) in KCs enhanced the production of proinflammatory cytokines.

3 is positively correlated with expression of proinflammatory cytokines.

4 esulting in the generation of high levels of proinflammatory cytokines.

5 r thickness and increased mRNA levels of key proinflammatory cytokines.

6 versible cell cycle arrest, and secretion of proinflammatory cytokines.

7 sferase activity, and expression analyses of proinflammatory cytokines.

8 els of neurotoxic TNFalpha and several other proinflammatory cytokines.

9 onocyte subsets, and an increase in systemic proinflammatory cytokines.

10 5' untranslated exons (UTRs), promoters, and proinflammatory cytokines.

11 oordinate the transcription and synthesis of proinflammatory cytokines.

12 or by targeting signaling initiated by other proinflammatory cytokines.

13 ator to enhance the transcription of several proinflammatory cytokines.

14 ways that eventually led to the secretion of proinflammatory cytokines.

15 autophagy's function in hepatotoxicity from proinflammatory cytokines.

16 l and activation, and promotes production of proinflammatory cytokines.

17 respond to extracellular IL-17A by inducing proinflammatory cytokines.

18 haracterized by production of type 1 IFN and proinflammatory cytokines.

19 avioral factors were related to increases in proinflammatory cytokines.

20 ll as fewer DEP exposure-induced circulating proinflammatory cytokines.

21 uce transcription of cortical or hippocampal proinflammatory cytokines.

22 zomib, do not effectively downregulate these proinflammatory cytokines.

23 PTSD symptom trajectory class membership on proinflammatory cytokines.

24 SCs treated recipients showed down-regulated proinflammatory cytokines.

25 lence of the virus, through induction of key proinflammatory cytokines.

26 e and reduced expression of neurodestructive proinflammatory cytokines.

27 nd that considered to be induced by multiple proinflammatory cytokines.

28 ed dendritic cells to release high levels of proinflammatory cytokines, a behavior we linked to xylos

29 Physiologically, proinflammatory cytokines activate ITCH to maintain BRAF

30 ith tranexamic acid delayed up-regulation of proinflammatory cytokines after APAP overdose.

31 equired for NF-kappaB-dependent induction of proinflammatory cytokines after FcepsilonR1 stimulation

32 were independent of bystander activation by proinflammatory cytokines after heterologous infection.

33 signaling cascade and enhance production of proinflammatory cytokines after stimulation with the TLR

34 ophagocytic phenotype but also tempers their proinflammatory cytokine and ferritin secretion by negat

35 ficient mice exhibit increased expression of proinflammatory cytokines and a higher frequency of deat

36 In addition, baseline levels of proinflammatory cytokines and behavioral measures predic

37 residual CTII and elevated concentrations of proinflammatory cytokines and cells were present in all

38 that was accompanied by the reduction of key proinflammatory cytokines and changes in plaque morpholo

39 tures had a molecular signature dominated by proinflammatory cytokines and chemokine induction, inclu

40 ls, and the local and systemic production of proinflammatory cytokines and chemokines (IL-1beta, IL-5

41 ociated with reduced levels in the plasma of proinflammatory cytokines and chemokines and lower level

42 PB caused major shifts in the expression of proinflammatory cytokines and chemokines in the colon an

43 ate immune system, causing the appearance of proinflammatory cytokines and chemokines, along with the

44 les in multiple sclerosis (MS): secretors of proinflammatory cytokines and chemokines, presenters of

45 the production of TNF-alpha- and STS-induced proinflammatory cytokines and chemokines.

46 icroenvironment, enhancing the production of proinflammatory cytokines and chemokines.

47 matory cells and the decreased production of proinflammatory cytokines and chemokines.

48 reased levels of GSH and decreased levels of proinflammatory cytokines and could potentially reduce t

49 male mice, promoting passage of circulating proinflammatory cytokines and depression-like behaviors.

50 ic effects of C5aR2 in increasing intestinal proinflammatory cytokines and enhancing circulating neut

51 gal response translates to the expression of proinflammatory cytokines and highlights an additional l

52 ith CaMKIV activation, as does expression of proinflammatory cytokines and histologic features of col

53 embly drives the maturation and secretion of proinflammatory cytokines and induces pyroptosis.

54 y enhances RIG-I mediated production of both proinflammatory cytokines and interferons.

55 gal burden, increased lung concentrations of proinflammatory cytokines and neutrophil-attracting chem

56 hamsters, in association with enrichment of proinflammatory cytokines and NO.

57 The proinflammatory cytokines and oxidized low-density lipop

58 It also decreases gene expression of proinflammatory cytokines and preserves mitochondria fun

59 Relative gene expressions of proinflammatory cytokines and proinsulin of the graft-be

60 c cells (DCs) release interferons (IFNs) and proinflammatory cytokines and promote adaptive immunity

61 nhibition of p38 suppressed the secretion of proinflammatory cytokines and promoted autophagy in BV2

62 pffer cells (KCs) enhances the production of proinflammatory cytokines and promotes the development o

63 riodontitis rats with a lower serum level of proinflammatory cytokines and reduced IL-17A(+) cells in

64 aspartate aminotransferase levels as well as proinflammatory cytokines and reduced the expression of

65 STAT3 appears to repress the expression of proinflammatory cytokines and restrict immune cell infil

66 tigen presentation to T cells, production of proinflammatory cytokines and secretion of anti-inflamma

67 ctive) transcriptional response and suppress proinflammatory cytokines and signaling pathways (i.e.,

68 Intracellular proinflammatory cytokines and SIRT1 were measured in blo

69 primary CML cells, resulting in secretion of proinflammatory cytokines and specifically killing in vi

70 h from OXPHOS and show reduced production of proinflammatory cytokines and the ability to activate T

71 We observed differences in proinflammatory cytokines and the relative proportion of

72 Interleukin (IL)-17, a proinflammatory cytokine, and T helper (Th)17 cells are

73 cies of activated/effector T cells producing proinflammatory cytokines, and an elevated T cell activa

74 thelial gut damage, bacterial translocation, proinflammatory cytokines, and betaDG-specific receptor

75 into host cells, eliciting the production of proinflammatory cytokines, and enhancing the translocati

76 reg cells are suppressive, unable to produce proinflammatory cytokines, and exhibit the epigenetic mo

77 mune cell infiltrates, reduced production of proinflammatory cytokines, and less lung-epithelial cell

78 receptor promotes inflammatory infiltrates, proinflammatory cytokines, and reactive oxygen species p

79 tenuated inflammasome-mediated production of proinflammatory cytokines, apoptosis, and pyroptosis, as

80 baumannii replicates significantly, and host proinflammatory cytokines are considerably reduced.

81 STAT5b expression determines if PRR-induced proinflammatory cytokines are increased or decreased, de

82 Although activating receptor engagement and proinflammatory cytokines are required to drive NK cell

83 ign is based on the idea that, if the excess proinflammatory cytokines are sequestered from the site

84 ronchoalveolar lavage fluid immune cells and proinflammatory cytokines as well as fewer DEP exposure-

85 ng cytokine, IL-12, and increased release of proinflammatory cytokines, as well as the anti-inflammat

86 he inflammasome modulates the release of key proinflammatory cytokines associated with periodontal di

87 beta-blocker use was associated with a more proinflammatory cytokine balance.Conclusions: Norepineph

88 Increased secretion of proinflammatory cytokines by macrophages in metabolic ti

89 uman leukocyte antigen class DR (HLA-DR) and proinflammatory cytokines by myeloid cells as well as im

90 ticular, NKG2D promotes higher production of proinflammatory cytokines by Th1 and T-bet+ Th17 cells a

91 ivation (CD4, CD8, CD25, CD62L and CD69) and proinflammatory cytokines (CCL2, CCL5, IL2, CXCL3, IFNga

92 ransient but robust IFN-gamma burst within a proinflammatory cytokine/chemokine landscape, transactiv

93 complexes caused significant upregulation of proinflammatory cytokine/chemokine transcripts and resul

94 nt evidence suggests that interactions among proinflammatory cytokines, chemokines, and cancer cell-r

95 proliferation and the secretion of a set of proinflammatory cytokines, chemokines, and growth factor

96 9-THC potently induces IL-10, while reducing proinflammatory cytokines, chemokines, and related organ

97 ibited significantly increased levels of the proinflammatory cytokines/chemokines IL-1beta, CXCL1, CX

98 Also, infected ECD mice elicited higher proinflammatory cytokines compared to mice under normal

99 cient CAR T cells produced higher amounts of proinflammatory cytokines compared with WT CAR T cells.

100 Proinflammatory cytokines directly modulate RANKL/OPG ex

101 ion of secondary effector molecules (such as proinflammatory cytokines) during bystander activation.

102 in vitro, thereby inducing the expression of proinflammatory cytokines (eg, TNF) and chemokines (eg,

103 , leukocyte apoptosis, and the production of proinflammatory cytokines, especially IL-1beta.

104 In vivo proinflammatory cytokine expression analysis and histopa

105 Surprisingly, infection induced robust proinflammatory cytokine expression and myeloid cell inf

106 /III IFN responses correlated with increased proinflammatory cytokine expression and with lung inflam

107 Taken together, reducing proinflammatory cytokine expression in the cerebral tiss

108 n (theophylline) upregulate SIRT1 and reduce proinflammatory cytokine expression in these cells.

109 Here we show that proinflammatory cytokine expression, chemokine expressio

110 Proinflammatory cytokine expression, including IL-1beta

111 stently IGRA-negative contacts produced more proinflammatory cytokines following heterologous stimula

112 RSV on various effect of TNF-alpha, a major proinflammatory cytokine for periodontitis and atherogen

113 IL-17A is a critical proinflammatory cytokine for the pathogenesis of asthma

114 ration enhanced PBMC respiration and reduced proinflammatory cytokine gene expression in 4 subjects w

115 n as measured by the F4/80 staining area and proinflammatory cytokine gene expression.

116 th reduced respiratory capacity and elevated proinflammatory cytokine gene expressions.

117 Proinflammatory cytokine genes were upregulated only for

118 subset of genes including p21(WAF1/CIP1) and proinflammatory cytokine genes, increased putative hepat

119 IL-17, a potent proinflammatory cytokine, has been shown to intimately c

120 ous IL-2 promoted IL-10(+) cells coproducing proinflammatory cytokines, higher IL-2 doses, both alone

121 re were significant reductions in intestinal proinflammatory cytokines, highlighting complicated dual

122 These phenomena were dependent on the proinflammatory cytokine IFN-gamma, which was required d

123 entrations and attenuated the release of the proinflammatory cytokine IFN-gamma-induced protein 10.

124 were proliferating (Ki67+) and producing the proinflammatory cytokines IFN-gamma and IL-17 in situ.

125 ndent manner and decrease the release of the proinflammatory cytokine, IFN-gamma.

126 ved to produce >10-fold higher levels of the proinflammatory cytokine IL-17 after stimulation with gr

127 The proinflammatory cytokine IL-1beta has been implicated in

128 adipose tissue (VAT) promotes release of the proinflammatory cytokine IL-1beta in obesity.

129 We previously demonstrated that a proinflammatory cytokine IL-1beta reduced the level of H

130 f severe influenza A pneumonia, we found the proinflammatory cytokine IL-6 was necessary for the deve

131 significantly decrease the secretion of the proinflammatory cytokine IL-6, and, via intra-articular

132 enic Th17 cells led to reduced expression of proinflammatory cytokines IL-17A, IFN-gamma, IL-22, and

133 Gene expression of proinflammatory cytokines IL-18 and IL-6 and phosphoryla

134 flammatory cytokine IL-37, as well as of the proinflammatory cytokines IL-18 and TNF, is increased in

135 ected skin to induce neutrophil recruitment, proinflammatory cytokines IL-1alpha, IL-1beta, and TNF,

136 tivate caspase-1 and drive the maturation of proinflammatory cytokines IL-1beta and IL-18.

137 ated pyroptotic cell death and maturation of proinflammatory cytokines IL-1beta and IL-18.

138 s inflammasome activation and release of the proinflammatory cytokines IL-1beta and IL-18.

139 ompts the caspase-1-mediated cleavage of the proinflammatory cytokines IL-1beta and IL-18.

140 However, high amounts of PGE(2) and the proinflammatory cytokines IL-1beta and IL-6 were secrete

141 other key finding is that NT, as well as the proinflammatory cytokines IL-1beta and TNF increase IL-3

142 ced THP-1 monocyte model, VR23 downregulates proinflammatory cytokines IL-1beta, TNF-alpha, IL-6, and

143 tion, and inhibited the transcription of the proinflammatory cytokines IL-6beta, COX2, iNOS, and IL-6

144 endent invasion induced the secretion of the proinflammatory cytokines IL-8 and CXCL1, which are asso

145 e inflammation by reducing the expression of proinflammatory cytokines (IL [interleukin]-1beta, IL-6,

146 ntly limited IFN response, the expression of proinflammatory cytokines (IL-6, IL-8) in NiV-infected P

147 )S levels resulted from the induction of the proinflammatory cytokine, IL-1beta, which is a pathologi

148 Another proinflammatory cytokine, IL-23, is critical for the dev

149 inflammation by activating the secretion of proinflammatory cytokines, IL-1beta and IL-18.

150 , we demonstrate that PDA tumor cell-derived proinflammatory cytokine IL1beta is essential for the es

151 g a 21-day exposure to IL-1beta, an abundant proinflammatory cytokine in the at-risk for lung cancer

152 f rheumatoid arthritis (RA) and TNF-alpha, a proinflammatory cytokine in the rheumatoid joint, facili

153 tion of activation markers and production of proinflammatory cytokines in a similar manner to B. burg

154 main concurrent with increased expression of proinflammatory cytokines in adipocytes from obese indiv

155 dent way, shifting the balance from anti- to proinflammatory cytokines in antimycobacterial responses

156 Although the importance of proinflammatory cytokines in controlling M. tuberculosis

157 Increased levels of proinflammatory cytokines in CS and vaping individuals m

158 the ability of S. aureus to induce ULBP2 and proinflammatory cytokines in human monocytes depends on

159 ed the ability of dendritic cells to produce proinflammatory cytokines in response to H. pylori While

160 having a role in DNA sensing, PYHIN1 induced proinflammatory cytokines in response to interleukin-1 (

161 Expression levels of proinflammatory cytokines in the CNS and induction of va

162 the bactericidal activity and generation of proinflammatory cytokines in the presence of S. aureus b

163 Finally, expression dysregulation of proinflammatory cytokines in the serum, including interl

164 gnificantly increased the gene expression of proinflammatory cytokines in the SP5 and SFO.

165 ectin-8-induced expression of chemokines and proinflammatory cytokines in the SUM159 breast cancer ce

166 ike (CIML) NK cells generated in response to proinflammatory cytokines in vitro and in vivo can also

167 which encodes a critical anti-proliferative, proinflammatory cytokine, in response to HCMV or dsDNA i

168 S-induced YAP further enhances expression of proinflammatory cytokines (including monocyte chemoattra

169 nsion carriers, we found increased levels of proinflammatory cytokines, including IL-17, and increase

170 fection is associated with the production of proinflammatory cytokines, including IL-17A.

171 lls and macrophages that excessively produce proinflammatory cytokines, including interferon-gamma (I

172 ses gene expression and systematic levels of proinflammatory cytokines, including interleukin (IL)-1b

173 s and counter-regulating macrophage-secreted proinflammatory cytokines, including migration inhibitor

174 REST reduced Mn-induced proinflammatory cytokines, including tumor necrosis fact

175 ted disorder involving systemic elevation of proinflammatory cytokines, including vIL-6 and human IL-

176 Proinflammatory cytokines increased with combinational t

177 e to suppress beta-cell apoptosis induced by proinflammatory cytokines, increasing the possibility th

178 ciated with elevated levels of TH1, TH2, and proinflammatory cytokines, indicating an association wit

179 e infection on tolerance is mainly driven by proinflammatory cytokines induced shortly after the infe

180 ted IFN production, but not IFN signaling or proinflammatory cytokine induction.

181 functions while retaining the capability of proinflammatory cytokine induction.

182 temic inflammation with high levels of serum proinflammatory cytokines, inflammatory infiltrates in v

183 Furthermore, proinflammatory cytokines inhibit steady-state erythropo

184 ease in anti-inflammatory cytokines, whereas proinflammatory cytokines initially decreased but then i

185 The proinflammatory cytokine interferon-gamma (IFN-gamma) ha

186 prehensive data set of 30 MeONPs to screen a proinflammatory cytokine interleukin (IL)-1 beta (IL-1be

187 st cells to respond to infection, expressing proinflammatory cytokine interleukin 6 (IL6) mRNA, which

188 rotein 6 (BMP6)/SMAD1/5/8 pathway and by the proinflammatory cytokine interleukin 6 (IL6).

189 he nucleus to the cytosol in response to the proinflammatory cytokine interleukin-6 (IL-6), suggestin

190 K9 concentrations negatively correlated with proinflammatory cytokine interleukin-8.

191 The immunological evaluation analyzed the proinflammatory cytokines interleukin-1 beta (IL-1beta),

192 dritic cells, and an increased production of proinflammatory cytokines (interleukin-12, interferon-ga

193 , more profound weight loss, increased serum proinflammatory cytokines (interleukin-17A, TNF, interle

194 with hourly assessment of depressed mood and proinflammatory cytokines (interleukin-6 (IL-6); tumor n

195 logy, in part, through the production of two proinflammatory cytokines: interleukin-17 (IL-17) and GM

196 or triggering several pathways that activate proinflammatory cytokines involved in alcohol-induced li

197 tes/Bacteroidetes (F/B ratio) and intestinal proinflammatory cytokines is significantly increased in

198 ficiency significantly reduced the levels of proinflammatory cytokines KC, IP-10, and IL-33 in bronch

199 otoxic degranulation, release granzyme B and proinflammatory cytokines, leading to target cell killin

200 d anti-inflammatory cytokines and attenuated proinflammatory cytokine levels.

201 erences observed in the expression levels of proinflammatory cytokines like tumor necrosis factor alp

202 tudies suggest that TNFalpha, IL-6 and other proinflammatory cytokines may mediate the feedback modul

203 ammatory in most settings, downregulates the proinflammatory cytokine microenvironment through modula

204 rane conductance regulator anion channels or proinflammatory cytokines might alter the paracellular p

205 MSCs reduced stress-induced circulating proinflammatory cytokines, monocytes, neuroinflammation,

206 associations include the negative effects of proinflammatory cytokines on monoaminergic neurotransmis

207 t with neutralizing antibodies against these proinflammatory cytokines or their receptors to inhibit

208 accumulation of donor-derived T cells with a proinflammatory cytokine phenotype in the colon.

209 eservation in SOM also significantly reduced proinflammatory cytokine production and release followin

210 2-DG inhibits proinflammatory cytokine production by MDM and monocyte-

211 ind Fc receptors on myeloid cells and induce proinflammatory cytokine production by monocytes and NET

212 in the nucleus for NF-kappaB activation and proinflammatory cytokine production during infection.

213 lable PDE4 inhibitor, on endotoxin-inducible proinflammatory cytokine production ex vivo in whole blo

214 logies and a coordinated reduction in spleen proinflammatory cytokine production in 17-month-old mice

215 g the first 48 h after transplantation drive proinflammatory cytokine production in conventional T ce

216 for Dectin-induced anti-fungal signaling and proinflammatory cytokine production in myeloid cells.

217 requirement of glycolytic reprogramming for proinflammatory cytokine production in normoxia is not o

218 (RSV) infection has been linked to enhanced proinflammatory cytokine production that promotes a Th2-

219 findings suggest a switch from predominantly proinflammatory cytokine production to chemokine product

220 normoxic conditions, only marginally affects proinflammatory cytokine production triggered through NO

221 ase of metabolically active enzymes, loss of proinflammatory cytokine production, and acquisition of

222 creatinine, less histologic damage, reduced proinflammatory cytokine production, and diminished prod

223 glucose transporter 1 (Glut1) expression for proinflammatory cytokine production, especially IL-1beta

224 ase inactivation on innate immune-associated proinflammatory cytokine production, including IL-1beta

225 owing exposure to DEPs, leading to increased proinflammatory cytokine production, reduced phagocytic

226 lycolysis, which is considered important for proinflammatory cytokine production.

227 romised chemotaxis, NFkappaB activation, and proinflammatory cytokine production.

228 ed PTEN and suppressed mTORC1 activation and proinflammatory cytokine production.

229 t of anti-inflammatory genes and dampens the proinflammatory cytokine profile through PI3K-mediated d

230 nery in the endoplasmic reticulum and Golgi, proinflammatory cytokines promote the modification of en

231 ion of TNFalpha, IL6 and IL12/IL23 (IL12p40) proinflammatory cytokines (PV = 0.0045, 0.0330, <0.0001,

232 In INS-1E cells and rat and human islets, proinflammatory cytokines reduced the content of SKAP2.

233 drome coronavirus 2 (SARS-CoV-2), amplifying proinflammatory cytokine release and acute phase respons

234 Exacerbated proinflammatory cytokines release (cytokine storm) and l

235 o viral clearance, but prolonged exposure to proinflammatory cytokines released during neuroinflammat

236 ral activity in the presence of a functional proinflammatory cytokine response might be one of the sp

237 way epithelial cell cultures induce a strong proinflammatory cytokine response yet block the producti

238 d NF-kappaB and ATF-4 as key drivers of this proinflammatory cytokine response.

239 CD14(+) monocytes with ONX 0914, diminished proinflammatory cytokine responses, thereby reducing the

240 lpha (TNF-alpha) as the key aging-associated proinflammatory cytokine responsible for platelet hyperr

241 they show enhanced expression of a cohort of proinflammatory cytokines, resulting in differentiation

242 Here we show that exposure to proinflammatory cytokines reveals a marked plasticity of

243 cts as an inflammation trap and captures the proinflammatory cytokines secreted at the implant site a

244 of FcgammaRIIIA (CD16) and by high levels of proinflammatory cytokine secretion and cytotoxic activit

245 and TLR4 localization to phagosomes, reduces proinflammatory cytokine secretion, abolishes phagosomal

246 rophage bacterial clearance and downregulate proinflammatory cytokine secretion.

247 athogenic T-helper type 1 (T(H)1) cells with proinflammatory cytokine secretion.

248 easured intracellular bacterial survival and proinflammatory cytokine secretion.

249 These same synovial fluid samples contain proinflammatory cytokines, similar to those produced by

250 thecal administration of an inhibitor of the proinflammatory cytokine soluble tumor necrosis factor a

251 Upon stimulation with proinflammatory cytokines such as tumor necrosis factor-

252 es mellitus, via the increased production of proinflammatory cytokines such as tumor necrosis factor-

253 the DeltafakA mutant has decreased levels of proinflammatory cytokines, such as interleukin-17A (IL-1

254 :C, resulting in increased production of key proinflammatory cytokines, such as TNF and IL-1beta.

255 d osteoclast formation and the expression of proinflammatory cytokines, such as tumor necrosis factor

256 ce of circulating poikilocytes, and elevated proinflammatory cytokines suggest inflammation-induced d

257 soy PG alone enhanced the expression of some proinflammatory cytokines, suggesting a narrow therapeut

258 pondin-1 (THBS1/TSP1), an antiangiogenic and proinflammatory cytokine that promotes insulin resistanc

259 ry subset of CD4(+) T cells, produce several proinflammatory cytokines that activate innate immune ce

260 henotype that includes the overproduction of proinflammatory cytokines that are toxic to cultured neu

261 pathologic role of IL-1alpha, one of the two proinflammatory cytokines that bind to IL-1R.

262 ine immune cells and inhibits the release of proinflammatory cytokines that cause the neuroinflammato

263 of chronic plaque psoriasis by inhibition of proinflammatory cytokines that require TYK2 and Janus ki

264 microdissected islets for gene expression of proinflammatory cytokines, the proliferation marker prol

265 Additionally, when combined with microglial proinflammatory cytokines, these exosomes further increa

266 The strong proinflammatory cytokine TNF-alpha (TNF) induces an acut

267 IVIg-FUS include the down-regulation of the proinflammatory cytokine TNF-alpha in the hippocampus.

268 state erythropoiesis in the bone marrow, the proinflammatory cytokines TNF-alpha and IL-1beta promote

269 loss (P <0 .01) and suppressed the levels of proinflammatory cytokines (TNF-alpha and IL-1beta), oxid

270 ignificantly induced IFN-alpha2a, IFN-gamma, proinflammatory cytokines (TNF-alpha, IL-2, IL-12p70), a

271 to this vaccine revealed the upregulation of proinflammatory cytokines (TNF-alpha, IL-6, and IL-1beta

272 ism whereby sustained stimulation by a major proinflammatory cytokine, TNF-alpha, regulates skeletal

273 The proinflammatory cytokine TNFalpha is elevated >3-fold in

274 zheimer's disease.SIGNIFICANCE STATEMENT The proinflammatory cytokine TNFalpha is known to be capable

275 Here, we demonstrate that the proinflammatory cytokine TNFalpha stimulates matrix meta

276 brains, with some continuing to express the proinflammatory cytokine TNFalpha.

277 lymphangiogenic growth factor VEGFD and the proinflammatory cytokine TNFalpha.

278 ors and induce type I interferons as well as proinflammatory cytokines to orchestrate an innate immun

279 motile Vibrio cells induce expression of the proinflammatory cytokine tumor necrosis factor alpha (TN

280 lso attenuated LPS-induced production of the proinflammatory cytokine tumor necrosis factor-alpha (TN

281 Proinflammatory cytokines tumor necrosis factor-alpha, I

282 at 7-months-of-age, the innate activation of proinflammatory cytokines (tumor necrosis factor alpha (

283 f aerated tissue, an increased production of proinflammatory cytokines (tumor necrosis factor-alpha).

284 ell interactions, we present evidence that a proinflammatory cytokine, tumor necrosis factor (TNF), c

285 allenge completely abrogated ERD, preventing proinflammatory cytokine upregulation and the infiltrati

286 ted the expression of various chemokines and proinflammatory cytokines via AKT activation, but there

287 urface TLR4 engagement predominantly induces proinflammatory cytokines via the signaling adaptor MyD8

288 Further studies demonstrated that proinflammatory cytokines, via suppression of COUP-TFII

289 Ex vivo production of proinflammatory cytokines was higher in PHEO patients.

290 to findings in adipose tissue, expression of proinflammatory cytokines was increased in liver and ske

291 o measured, and a reduction in the levels of proinflammatory cytokines was observed following STI tre

292 L-1) blocks the production of IL-6 and other proinflammatory cytokines, we treated COVID-19 patients

293 Increases in levels of proinflammatory cytokines were associated with both tiss

294 phils, and lymphocytes) and higher levels of proinflammatory cytokines were found in Spp1(-/-) mice t

295 4 activation, resulting in the activation of proinflammatory cytokines, which drives morphine toleran

296 ells are characterized by an upregulation of proinflammatory cytokines, which is termed the senescenc

297 Traumatic brain injury increases proinflammatory cytokines, which trigger excess function

298 inhibition reduces the secretion of several proinflammatory cytokines, with the suppression of IL-23

299 yelination, and reduced expression levels of proinflammatory cytokines within the neural tissue compa

300 Unexpectedly, celastrol upregulated proinflammatory cytokines without affecting genes involv