ライフサイエンスコーパス: proinflammatory

1 cators of macrophage polarization towards M1/proinflammatory.

2 -GlcNAc) signaling in suppressing macrophage proinflammatory activation and preventing diet-induced m

3 echanisms by which PARPs promote or suppress proinflammatory activation of macrophages, and various r

4 ignaling is down-regulated during macrophage proinflammatory activation.

5 ution that has pleiotropic effects on S100A9 proinflammatory activity and proteolytic resistance but

6 toxicity, including membranolysis, in vitro proinflammatory activity, and lung inflammation.

7 eveal the Abeta-burdened neuron as a primary proinflammatory agent, implicating the intraneuronal acc

8 ry AM was decreased, whereas CD163(-)CCR7(+) proinflammatory AM were increased in HIV infection.

9 that while ITx rejection is associated with proinflammatory and activated effector memory T cells in

10 ing in macrophages regulates a shift between proinflammatory and anti-inflammatory activation during

11 tes the dynamics of macrophage infiltration, proinflammatory and anti-inflammatory cytokine expressio

12 on of amyloid deposits, and normalization of proinflammatory and anti-inflammatory cytokine productio

13 w insights into the metabolism dependency of proinflammatory and anti-inflammatory ILC2 phenotypes.

14 ch may be synthesized from GLA and result in proinflammatory and anti-inflammatory metabolites, respe

15 a peripheral "vascular storm," with elevated proinflammatory and antiviral mediators and the influx o

16 diac pathology with less inflammation, lower proinflammatory and chemotactic cytokines, less interleu

17 ion, lowered the level of AGEs, and improved proinflammatory and fibrogenic responses in mice on a hi

18 oxygen stable HIF1alpha reversed attenuated proinflammatory and glycolytic gene expression in KLF6-d

19 Paradoxically, senescent cells secrete proinflammatory and growth-stimulatory molecules, termed

20 GPR84 is expressed on immune cells mediating proinflammatory and immunostimulatory effects.

21 and cell adhesion as well as induction of a proinflammatory and proadipogenic signature in endotheli

22 tomic profile of high expression of combined proinflammatory and profibrotic genes are associated wit

23 The injured tubules acquired a proinflammatory and profibrotic phenotype; moreover, AKI

24 of endomyocardial biopsies reveals a strong proinflammatory and profibrotic signature in the hearts

25 fection inhibits NFkappaB, thereby dampening proinflammatory and prosurvival signals.

26 of extracellular histones, which are highly proinflammatory and prothrombotic.

27 so observed a skewing in the balance between proinflammatory and regulatory T cells potentially favor

28 es such as CXCL10, CYP7B1, and corresponding proinflammatory and steroid biosynthetic gene networks,

29 enicity, if T cell stimulation occurred in a proinflammatory and TGF-beta-low cytokine microenvironme

30 has been implicated, along with other HHV-8 proinflammatory and/or angiogenic viral proteins, in HHV

31 JMJD2B, which is induced by EndMT-promoting, proinflammatory, and hypoxic conditions, and supports th

32 hylase JMJD2B is induced by EndMT-promoting, proinflammatory, and hypoxic conditions.

33 ne regulators (IDO1, SOCS3, and IL10), and a proinflammatory antimicrobial peptide (S100A7).

34 produced increased levels of acylcarnitines, proinflammatory arachidonic acid metabolites, cytokines,

35 st prevalent in CF, with a dominant immature proinflammatory archetype.

36 ost macrophage inflammatory responses to the proinflammatory beta -glucan components of the organisms

37 ociated with a higher circulating profile of proinflammatory biomarkers, lower levels of adiponectin,

38 First, Trem2(+) foamy macrophages are not proinflammatory but interferon-inducible cell and inflam

39 ammatory responses and may help to prevent a proinflammatory cascade.

40 althy controls, raising the possibility that proinflammatory CD151+ T cells could contribute to the p

41 etter living through chemicals' and limiting proinflammatory chemicals entering the body.

42 f this study was to image the recruitment of proinflammatory chemokine receptor 2-positive (CCR2+) ce

43 scarring progression included those encoding proinflammatory chemokines (CXCL5, CCL20, CXCL13, and CC

44 -deficient keratinocytes massively expressed proinflammatory chemokines and immunomodulatory proteins

45 the production of trimethylamine N-oxide, a proinflammatory compound associated with cardiovascular

46 Maturation of DCs induced by diverse proinflammatory conditions promotes immune responses, bu

47 Under proinflammatory conditions, endothelial cells can acquir

48 n primary human T(reg) cells under basal and proinflammatory conditions.

49 n gene-deficient mice had smaller numbers of proinflammatory cuffs, less extensive demyelination, and

50 ped discover that KSHV infection hijacks the proinflammatory cyclooxygenase-2 (COX-2) and 5-lipoxygen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 The proinflammatory cytokines and oxidized low-density lipop

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

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

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

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

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

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

104 Proinflammatory cytokines directly modulate RANKL/OPG ex

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

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

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

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

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

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

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

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

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

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

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

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

117 Exacerbated proinflammatory cytokines release (cytokine storm) and l

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

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

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

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

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

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

124 Proinflammatory cytokines tumor necrosis factor-alpha, I

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 zomib, do not effectively downregulate these proinflammatory cytokines.

147 PTSD symptom trajectory class membership on proinflammatory cytokines.

148 SCs treated recipients showed down-regulated proinflammatory cytokines.

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

150 e and reduced expression of neurodestructive proinflammatory cytokines.

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

152 ator to enhance the transcription of several proinflammatory cytokines.

153 autophagy's function in hepatotoxicity from proinflammatory cytokines.

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

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

156 vated conventional CD4+ T cells (Tconvs) and proinflammatory dendritic cells (DCs), which are both im

157 ventricle manifested by lowered abundance of proinflammatory detrimental neutrophils.

158 ings suggest that a maternal low-quality and proinflammatory diet may increase the risk of emotional

159 ors, a higher E-DII score, indicating a more proinflammatory diet, was associated with higher risk of

160 This study sought to examine whether proinflammatory diets are associated with increased CVD

161 g of human glycan-targeting IgG1 mAb confers proinflammatory direct cell killing and enhanced avidity

162 d effector functions, paving the way for the proinflammatory direct cell killing to promote antibody-

163 A proinflammatory dysregulation of cytokine release is ass

164 erentiation and mineralization and exerted a proinflammatory effect on cementoblasts.

165 osed in which non-nicotinic elements exert a proinflammatory effect that is functionally antagonized

166 xidation pathway conventionally utilized for proinflammatory effector functions.

167 tissue-resident leukocytes that have potent proinflammatory effects in a number of diseases.

168 that can target MAC assembly, signaling, and proinflammatory effects in various complement-mediated d

169 Thus, the proinflammatory effects of RBP4 require NLRP3-inflammaso

170 carrier in serum, is elevated in AT and has proinflammatory effects which are mediated partially thr

171 a and IFN-beta responses can lead to harmful proinflammatory effects, whereas IFN-lambda mainly signa

172 We measured SPMs and proinflammatory eicosanoid levels using liquid chromatog

173 Although proinflammatory eicosanoids, including prostaglandins, t

174 A depletion of proinflammatory elastase-related proteases in neutrophil

175 1, in conjunction with the severe endogenous proinflammatory environment, can convert defective Treg

176 ine (RAW264.7); however, DOPG was not itself proinflammatory even at high concentrations.

177 ived signal and responds by downregulating a proinflammatory factor (T3SS1), thus enhancing intestina

178 microbiota-dependent increased expression of proinflammatory factors and decreased expression of the

179 Concomitantly, the production of proinflammatory factors such as TNFalpha, IL1beta and TG

180 Although CF monocytes exhibited proinflammatory features, both monocytes and neutrophils

181 Necroptosis is a proinflammatory form of cell death instigated by pore-fo

182 offspring were accompanied by reductions in proinflammatory gene expression in liver and WAT and inc

183 increased inflammatory cell infiltration and proinflammatory gene expression in the liver, which was

184 hough CGRP receptor blockade reduced certain proinflammatory gene expression, bacterial burden and Il

185 TonEBP/NF-kappaB p65 complexes and enhanced proinflammatory gene expression.

186 mediated a repressive chromatin state of the proinflammatory gene promoter as a result of decreased a

187 ng in robust ligand-independent induction of proinflammatory genes and oncogenes.

188 remarkable lack of significant induction of proinflammatory genes classically implicated in primate

189 neuroprotective genes with downregulation of proinflammatory genes in Group 1 in comparison to Group

190 xpression of interferon-associated genes and proinflammatory genes in infected hAT2 cells, indicating

191 isol exposure, mediating the upregulation of proinflammatory genes that we reported previously.

192 XCL8, tumor necrosis factor (TNF), and other proinflammatory genes.

193 on homeostatic (M-CSF, TGF-beta-treated) and proinflammatory (GM-CSF-treated) human monocyte-derived

194 as may form due to pre-existing CKD; and (3) proinflammatory granuloma-related M1-like macrophages ma

195 lesterol efflux capacity values, pro-oxidant/proinflammatory HDL particles, and low HDL levels of sph

196 tigate the role of microRNA-155 (miR-155), a proinflammatory host innate immune regulator responsible

197 The disease progression associated with the proinflammatory host response prompted us to examine the

198 telet counting, and the quantification of 13 proinflammatory human chemokines/cytokines.

199 ility to autoimmune diseases acuminates in a proinflammatory IgG fraction crystallizable N-glycosylat

200 IL-36 cytokines are proinflammatory IL-1 superfamily members, yet their role

201 The proinflammatory immune response to Mtb infection in untr

202 he study findings suggest that assessing the proinflammatory immune response to trauma exposure immed

203 The overactive proinflammatory immune signatures offers targets for hos

204 endritic cells that are polarized to a mixed proinflammatory/immune-suppressive phenotype.

205 suggest that KDM6 expression in DC enhances proinflammatory innate cytokine production to promote an

206 ignificantly suppressed postnatal peripheral proinflammatory insult-induced systemic inflammation and

207 activation, caspase-1 (CASP1) cleavage, and proinflammatory interleukin 1beta (IL1B) maturation.

208 nd regulatory T cells potentially favoring a proinflammatory intrathecal environment in HTT gene expa

209 served during aging, including the excessive proinflammatory ligand-receptor interplay, were reversed

210 's and large LDL particles, as well as other proinflammatory lipids and stress hormones such as corti

211 Proinflammatory M1 macrophages can phagocytose tumor cel

212 UA crystal granulomas surrounded by proinflammatory M1-like macrophages developed late in th

213 particular, the shift of macrophages from a proinflammatory (M1 biased) phenotype to a proregenerati

214 tal signals polarize macrophages to either a proinflammatory (M1) state or an anti-inflammatory (M2)

215 inflammation and dysfunction, as assessed by proinflammatory macrophage accumulation.

216 ection, along with cigarette smoke, favors a proinflammatory macrophage phenotype associated with enh

217 FA/Ang2 and anti-CD40 independently promoted proinflammatory macrophage skewing and increased dendrit

218 Proinflammatory macrophages are important mediators of i

219 Because proinflammatory macrophages recruited to adipose tissue

220 Myeloid cells included 2 populations of proinflammatory macrophages showing IL (interleukin) 1B

221 e importance of TLR engagement in activating proinflammatory macrophages, relatively little is known

222 oth cell types expressed increased levels of proinflammatory markers: inducible nitric-oxide synthase

223 We propose that the LrS attenuates proinflammatory mediator expression through increased tr

224 ries" that are essential for the cleavage of proinflammatory mediator IL-1beta into an active form.

225 Leukotriene B4 (LTB4) is a major proinflammatory mediator important in host defense, wher

226 mplement activation fragment C5a is a potent proinflammatory mediator that is increasingly recognized

227 neutrophils upregulate SEMA3F in response to proinflammatory mediators and following neutrophil recru

228 se autoallergens, which provoke a release of proinflammatory mediators from skin mast cells.

229 TBI increased expression of proinflammatory mediators in the cortex and hippocampus

230 In control tissues, type 2/3 and proinflammatory mediators showed an inverse correlation

231 In addition, mRNA expression of proinflammatory mediators was increased, whereas markers

232 ramming was required to generate a number of proinflammatory mediators, including IL-1beta, and was d

233 inocytes, which can be stimulated to produce proinflammatory mediators.

234 of gammadelta T cells and the expression of proinflammatory mediators.

235 diated airway inflammation and expression of proinflammatory mediators.

236 Together, these findings decipher a proinflammatory metabolic and epigenetic reprogramming o

237 iabetes and the potential role played by the proinflammatory metabolic state in these patients that p

238 s) might have different sensitivities to the proinflammatory milieu generated by brain death.

239 sing mice exhibited diminished expression of proinflammatory molecules and had more F4/80(+) macropha

240 monocytes, with preferential binding to the proinflammatory monocyte subtype and partially via SR-BI

241 characterized by persistent accumulation of proinflammatory monocytes (Mo)/macrophages (MPhi) and im

242 Although repression of formoterol-induced proinflammatory mRNAs should be beneficial, the pathophy

243 Proinflammatory myeloid cells expressed high levels of C

244 regulates gut microbes, and dephosphorylates proinflammatory nucleotides.

245 t only identifies a novel psoriasis-relevant proinflammatory pathway, but also proposes the repurposi

246 players in the unfolded protein response and proinflammatory pathways associated with progression of

247 t intercalated cells (ICs) rapidly adopted a proinflammatory phenotype after IRI.

248 ly altered astrocyte biology, resulting in a proinflammatory phenotype and functional changes.

249 ated with HU were less efficient to induce a proinflammatory phenotype in ECs compared with MPs colle

250 role in SCD pathophysiology by triggering a proinflammatory phenotype of ECs.

251 tion potential, impaired self-renewal, and a proinflammatory phenotype.

252 cids are associated with an accumulation and proinflammatory polarization of macrophages within metab

253 ansferase (OGT) knockout enhances macrophage proinflammatory polarization, promotes adipose tissue in

254 ing sepsis, ECs shift toward a proapoptotic, proinflammatory, proadhesive, and procoagulant phenotype

255 lood biomarkers, DLB would show an increased proinflammatory profile compared with controls, and that

256 study for the first time shows the distinct proinflammatory profiles of macrophages are controlled b

257 ver disease by reestablishing a conventional proinflammatory program in innate immune cells and/or co

258 This protocol assesses proinflammatory properties of nucleic acid nanoparticles

259 ranscription factor Foxp3 and acquisition of proinflammatory properties(2), can promote autoimmunity

260 d transcripts, including those encoding many proinflammatory proteins, was repression.

261 C-activated cells have been found to express proinflammatory proteins-often through NF-kappaB-depende

262 nhibitor, AZ505, led to increased protective proinflammatory response and inhibited amastigote multip

263 the unfolded protein response (UPR) and the proinflammatory response associated with viral pathogene

264 n kinase (MAPK) signaling to elicit a robust proinflammatory response characterized by the secretion

265 taining the secretome, greatly decreased the proinflammatory response of primary macrophages and RAW

266 nd leukocyte recruitment along with limiting proinflammatory responses in macrophages.

267 WT mice, Clec2d(-/-) mice exhibited reduced proinflammatory responses to injected histones, and less

268 cell membrane rupture may incite deleterious proinflammatory responses, which can exacerbate local ti

269 g to the TNF superfamily and are involved in proinflammatory responses.

270 strointestinal syndromes, and a reduction in proinflammatory responses.

271 sis in regions associated with sepsis-driven proinflammatory responses.

272 We further characterized Nck1's proinflammatory role by identifying interleukin 1 type I

273 it is likely to disproportionately activate proinflammatory S1P(1) signaling, shifting the balance a

274 usability of aMMP-8 PoC test for predicting "proinflammatory" salivary profile and periodontal health

275 by a stable cell cycle arrest and a complex proinflammatory secretome, termed the senescence-associa

276 Here, we identified a novel proinflammatory signaling pathway driven by cyclin-depen

277 ation induced by heme were critical for most proinflammatory signaling pathways, as the antioxidant N

278 of GIV's TILL motif to TIR modules inhibits proinflammatory signaling via other TLRs, suggesting a c

279 rways disease by increasing IL-1beta-induced proinflammatory signaling, in part, through phosphorylat

280 of muscle wasting associated with sustained proinflammatory signaling.

281 mostly female group with smaller hearts and proinflammatory signaling.

282 cytokine capable of suppressing a number of proinflammatory signals associated with intestinal infla

283 and melanocytes of the anagen hair matrix of proinflammatory signals required for full oncogenic tran

284 acutely infected individuals induced a more proinflammatory signature than those from uninfected ind

285 A systemic proinflammatory state has been hypothesized to mediate t

286 This may be attributed to a pre-existing proinflammatory state that is further propelled with the

287 Transition of macrophages from a proinflammatory state to a reparative state, however, is

288 hift from a homeostatic to a multifunctional proinflammatory state.

289 to reduce the complications related to this proinflammatory state.

290 r the activation of Toll-like receptors with proinflammatory stimuli and that the upregulation of lip

291 The infection of cells activates proinflammatory substances, causing diffuse alveolar dam

292 n of key costimulatory molecules involved in proinflammatory T cell differentiation, including cluste

293 n bulk analyses, including those involved in proinflammatory T cell differentiation, prolonged monocy

294 These proinflammatory T cells promoted bacterial clearance aft

295 p3, TGF-beta, IL-10, and decreased levels of proinflammatory T-bet, IL-1beta, TNF-alpha, and IFN-gamm

296 We identified proinflammatory TNFalpha/NFkappaB signaling and hdac1 as

297 the induction of IkappaBzeta, which is a key proinflammatory transcription factor required for cytoki

298 both SP and its associated EVs elicit potent proinflammatory transcriptional responses in cells that

299 Programmed cell death 4 (PDCD4) is a proinflammatory tumor-suppressor gene which helps to pre

300 We discovered that a proinflammatory Vibrio symbiont native to zebrafish gove