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

1 on-gamma (IFN-gamma), generally considered a proinflammatory cytokine.

2 ractant, whereas a disulfide bond makes it a proinflammatory cytokine.

3 n of the thymic stromal lymphopoietin (TSLP) proinflammatory cytokine.

4 K signalling and increases the production of proinflammatory cytokines.

5 d profound uveal inflammation and release of proinflammatory cytokines.

6 related with enhanced expression of numerous proinflammatory cytokines.

7 ecific T cell proliferation and secretion of proinflammatory cytokines.

8 duced by macrophages induces upregulation of proinflammatory cytokines.

9 infection in response to local cDC1-derived proinflammatory cytokines.

10 ry smooth cells secrete IL-26 in response to proinflammatory cytokines.

11 ied regarding the induction of Th2, Th1, and proinflammatory cytokines.

12 eta activation that upregulates secretion of proinflammatory cytokines.

13 ment of inflammatory cells and production of proinflammatory cytokines.

14 e into effector T cells capable of producing proinflammatory cytokines.

15 having highly elevated levels of circulating proinflammatory cytokines.

16 markers of illness, and local production of proinflammatory cytokines.

17 ing plasmablasts in the presence of BAFF and proinflammatory cytokines.

18 n relation to the mRNA expression profile of proinflammatory cytokines.

19 that prevent phagocytosis and generation of proinflammatory cytokines.

20 a regulatory phenotype in vitro and secrete proinflammatory cytokines.

21 the mechanisms behind its downregulation by proinflammatory cytokines.

22 sult in aberrations in production of various proinflammatory cytokines.

23 s increase production of numerous additional proinflammatory cytokines.

24 microbial products through the synthesis of proinflammatory cytokines.

25 h17 cells, and produced increased amounts of proinflammatory cytokines.

26 endogenous CLIP170 potentiated the levels of proinflammatory cytokines.

27 LPS and promotes pyroptosis and secretion of proinflammatory cytokines.

28 se two signals cause the release of multiple proinflammatory cytokines.

29 lls promote IR, in part through secretion of proinflammatory cytokines.

30 osis factor (TNF) but had no effect on other proinflammatory cytokines.

31 ting levels of CXCL9, CXCL10, and downstream proinflammatory cytokines.

32 CD8(+) cells, alanine aminotransferase, and proinflammatory cytokines.

33 CD200R expression produced higher levels of proinflammatory cytokines.

34 on of T cell responses and the production of proinflammatory cytokines.

35 nt expression of type I interferon and other proinflammatory cytokines.

36 in increased production of type 2 and other proinflammatory cytokines.

37 ncluding Kupffer cells exposed to HCV induce proinflammatory cytokines.

38 signaling pathways leading to the release of proinflammatory cytokines.

39 -M, also known as IRAK-3, is an inhibitor of proinflammatory cytokine and chemokine expression in int

40 PM is associated with increased proinflammatory cytokine and chemokine levels in placent

41 IFNs but were associated with altered local proinflammatory cytokine and chemokine responses and dif

42 indings indicate that S100A12 functions as a proinflammatory cytokine and suggest that S100A12 is a p

43 ndent gene expression and down-regulation of proinflammatory cytokines and adhesion molecules.

44 antagonists of GHRH suppressed the levels of proinflammatory cytokines and altered the expression of

45 in and bryostatin-1 induce secretion of some proinflammatory cytokines and an increase of ICAM-1 expr

46 RA101295 abolished sepsis-induced surges in proinflammatory cytokines and attenuated systemic circul

47 t SCARF-1 expression by HSEC is regulated by proinflammatory cytokines and bacterial lipopolysacchari

48 esulting in caspase-1 activation, release of proinflammatory cytokines and cell death.

49 DENV induced expression of proinflammatory cytokines and chemokines by infected ker

50 ction significantly increasing the levels of proinflammatory cytokines and chemokines in the M1 versu

51 ted chemokine concurrent with an increase in proinflammatory cytokines and chemokines were seen after

52 Gal-3 treatment was accompanied by increased proinflammatory cytokines and chemokines within the loca

53 stable proliferation arrest and secretion of proinflammatory cytokines and chemokines, the senescence

54 hereas MIA produced significant increases in proinflammatory cytokines and chemokines.

55 This longitudinal study investigated proinflammatory cytokines and comorbidity development ov

56 The proinflammatory cytokines and extracellular apoptosis-as

57 s paralleled the decrease in serum levels of proinflammatory cytokines and ferritin.

58 very to the lung downregulates expression of proinflammatory cytokines and improves allergen-induced

59 Activation of Nlrp3 leads to synthesis of proinflammatory cytokines and influences epithelial inte

60 hese macrophage-like nanoparticles sequester proinflammatory cytokines and inhibit their ability to p

61 of infection, WT mice had higher circulatory proinflammatory cytokines and lower anti-inflammatory cy

62 nogenesis, we evaluated associations between proinflammatory cytokines and lung cancer risk.

63 NA expression as well as expression of other proinflammatory cytokines and mediators, including IL-1a

64 -cycle arrest combined with the secretion of proinflammatory cytokines and mitochondrial dysfunction.

65 duced sepsis, decreases the plasma levels of proinflammatory cytokines and organ injury markers in a

66 f atherosclerotic plaques, the production of proinflammatory cytokines and reactive oxygen species, t

67 e precipitating steps involve the release of proinflammatory cytokines and stress hormones, increased

68 glucocorticoid biosynthesis is suppressed by proinflammatory cytokines and that glucocorticoid defici

69 that BCA2 is induced by NF-kappaB-activating proinflammatory cytokines and that upregulation of BCA2

70 unity by changing the homeostatic balance of proinflammatory cytokines and the human immune system, i

71 urified sLRP1 induced expression of multiple proinflammatory cytokines and the mRNA encoding inducibl

72 mulated insulin secretion in the presence of proinflammatory cytokines and triggered gene expression

73 tion, and leukocyte migration plus genes for proinflammatory cytokines and various toll-like receptor

74 rentiation-associated genes, upregulation of proinflammatory cytokines, and accumulation of Langerhan

75 roteins, leading to increased levels of ROS, proinflammatory cytokines, and adhesion molecules in SCD

76 binding to TLR2 induced robust expression of proinflammatory cytokines, and end products of lipid oxi

77 emlin1 and R-spondin1 as well as chemokines, proinflammatory cytokines, and growth factors with key r

78 beta cells resistant to apoptosis induced by proinflammatory cytokines, and inhibition of autophagy w

79 reatment showed decreased mRNA expression of proinflammatory cytokines, and partially reversed TNF-al

80 traumatic insult), become activated, produce proinflammatory cytokines, and recruit monocytes and den

81 inflammatory cells with local production of proinflammatory cytokines, and subsequent epithelial dis

82 tical thinning was correlated with levels of proinflammatory cytokines at baseline.

83 mmation, accompanied by a massive release of proinflammatory cytokines at the maternal-fetal interfac

84 ion is associated with intense production of proinflammatory cytokines, but whether this cytokine sto

85 ens at various nonmucosal sites by eliciting proinflammatory cytokines by human macrophages, monocyte

86 these glycolipids induced the production of proinflammatory cytokines by macrophages, thereby sugges

87 While proinflammatory cytokines can be detected in the lungs a

88 (less cardiac infiltrates and suppression of proinflammatory cytokines), cardiac fibrosis, apoptosis,

89 l inflammation by inducing the expression of proinflammatory cytokines, chemokines and matrix metallo

90 mote pathophysiologic developments involving proinflammatory cytokines, chemokines, and adhesion mole

91 ation of many antiviral molecules, including proinflammatory cytokines, chemokines, and IFN-stimulate

92 ases 1 (TIMP-1), downregulated expression of proinflammatory cytokines/chemokines, and significantly

93 survival and decreased alveolar protein and proinflammatory cytokine concentrations, whereas increas

94 ninfected, TT-genotype patients had high CSF proinflammatory cytokine concentrations, with intermedia

95 Interferon gamma (IFNgamma) is the major proinflammatory cytokine conferring resistance to the in

96 tion of inflammation, including reduction of proinflammatory cytokines (CXCL1, CXCL2, CCL3, CCL4, IL6

97 tumors displayed elevated expression of the proinflammatory cytokine CXCL5.

98 on of TNF-alpha and IL-1beta, widely studied proinflammatory cytokines, did not induce persistent dis

99 Cholangiocytes secrete proinflammatory cytokines during bacterial infection lea

100 ungs and their relationship with circulating proinflammatory cytokines during ischemia-reperfusion in

101 m and hypothalamic mRNA responses of certain proinflammatory cytokines during the active phase.

102 also reduces chemotherapy-induced release of proinflammatory cytokines (e.g., TNFalpha), hypertrophic

103 phate nucleotidohydrolase induced SAMHD1 and proinflammatory cytokines (eg, interleukin 6, interleuki

104 Siglec-E16 enhanced proinflammatory cytokine expression and bacterial killin

105 Csn5 KO potentiated NF-kappaB signaling and proinflammatory cytokine expression in macrophages, wher

106 ed a mechanism by which Muller cells trigger proinflammatory cytokine expression in myeloid cells.

107 mediated induction of adhesion molecules and proinflammatory cytokine expression in response to LPS.

108 In addition, tapinarof moderates proinflammatory cytokine expression in stimulated periph

109 Moreover, increases in proinflammatory cytokine expression were also greatly at

110 tion, with increased histological scores and proinflammatory cytokine expression, compared to control

111 ion proteins, myosin light chain kinase, and proinflammatory cytokine expression.

112 The tumor microenvironment supplies proinflammatory cytokines favoring a permissive milieu f

113 phages results in the coordinated release of proinflammatory cytokines, followed by regulatory mediat

114 o, these dendrimers reduced the secretion of proinflammatory cytokines from mice and human monocyte-d

115 Consequently, sustained expression of proinflammatory cytokines from the epidermis is associat

116 nza virus-induced lethality and reduced both proinflammatory cytokine gene expression in the lungs an

117 7- to 2.1-fold increase in levels of several proinflammatory cytokines (GM-CSF, IFN-gamma, IL-1beta,

118 ng a mouse model of colitis, we identify the proinflammatory cytokine granulocyte-colony-stimulating

119 Proinflammatory cytokines, IFN-gamma and IL-17A, produce

120 Proinflammatory cytokines (IFNgamma, MCP1, MIP1alpha, an

121 r cytotoxic mediators (perforin/granzyme B), proinflammatory cytokines (IFNgamma/TNFalpha), and expre

122 ion between autoantibodies to troponin I and proinflammatory cytokine IL-18.

123 nonrelevant modifications of the prototypic proinflammatory cytokine IL-1beta during an immune respo

124 iated with reduced microglial activation and proinflammatory cytokine IL-1beta within the subfornical

125 ASC) and trigger caspase-1 processing of the proinflammatory cytokine IL-1beta.

126 The proinflammatory cytokine IL-36gamma is highly expressed

127 ated the canonical NF-kappaB pathway and the proinflammatory cytokine IL-6 in autoantibody production

128 naling potently repressed the release of the proinflammatory cytokine IL-6 in primary mouse HD and WT

129 At 6 h we detect the proinflammatory cytokine IL-6 in the hippocampus, follow

130 s microbial pathogens and then activates the proinflammatory cytokines IL-1 and IL-18.

131 , NRF2 induction repressed expression of the proinflammatory cytokines IL-1, IL-6, IL-8, and TNFalpha

132 f caspase-1 leading to the maturation of the proinflammatory cytokines IL-1beta and IL-18 and promoti

133 ensified NLRP3 activation, overproduction of proinflammatory cytokines IL-1beta and IL-18, and increa

134 ults in caspase-1-dependent secretion of the proinflammatory cytokines IL-1beta and IL-18.

135 le for caspase-1-dependent maturation of the proinflammatory cytokines IL-1beta and IL-18.

136 y suppress the production of the ILC2-driven proinflammatory cytokines IL-5 and IL-13 both in vitro a

137 R4 activation to limit the production of the proinflammatory cytokines IL-6 and IL-12p40 while enhanc

138 associated with decreased concentrations of proinflammatory cytokines (IL-1alpha, IL-8, IL-12(p70))

139 species (ROS) and upregulated expression of proinflammatory cytokines (IL-1beta and TNFalpha).

140 he incident visit and when concentrations of proinflammatory cytokines (IL-1beta, IL-12p70) were incr

141 ce exhibited significantly reduced levels of proinflammatory cytokines (IL-4, IL-5, and IL-13) and de

142 from ER stress - apoptosis, NF-kappaB (p65), proinflammatory cytokines (IL-6, IL-1beta), neutrophil c

143 dicate that FP7 antagonized the secretion of proinflammatory cytokines (IL-6, IL-8, and MIP-1beta) by

144 n to the brain and activation of the central proinflammatory cytokine, IL1.

145 emia was shown to promote gene expression of proinflammatory cytokines (il1beta, il6, il8, and tnfalp

146 25-3p and miR-92a-3p stimulated secretion of proinflammatory cytokine IL6 from tumor-associated macro

147 ma in situ (DCIS) increased secretion of the proinflammatory cytokine IL6.

148 The mRNA and protein expression levels of proinflammatory cytokines IL6, IL8 and CCL5 were determi

149 In vivo neutralization of these proinflammatory cytokines impaired bacterial clearance a

150 IL-34 is a proinflammatory cytokine implicated in rheumatoid arthri

151 TNF-alpha is a proinflammatory cytokine implicated in the pathogenesis

152 ng cause of pPROM due to increased levels of proinflammatory cytokines in amniotic fluid.

153 ice showed exacerbated lung inflammation and proinflammatory cytokines in an ozone-exposure model.

154 ased survival rates and heightened levels of proinflammatory cytokines in both peritoneal lavage and

155 The role of proinflammatory cytokines in cognitive function has been

156 te-phase proteins, inflammatory markers, and proinflammatory cytokines in individuals with (infected

157 was more strongly induced by stimulation of proinflammatory cytokines in keratinocytes and fibroblas

158 LCN2 modulated the secretion of proinflammatory cytokines in PSC of the PDAC tumor micro

159 he reduced capacity of leukocytes to release proinflammatory cytokines in response to ex vivo stimula

160 ound that Ndfip1 restricts production of the proinflammatory cytokines in Th17 cells.

161 d mononuclear cells (MMCs) and the levels of proinflammatory cytokines in the blood and the brains of

162 ruptures elicited sustained upregulation of proinflammatory cytokines in the fetal membranes.

163 ce of immune complexes and the production of proinflammatory cytokines in the kidneys and normal humo

164 -alpha and IL-1beta induced transcription of proinflammatory cytokines in the primary synoviocytes.

165 ned the effect of NRTIs on the expression of proinflammatory cytokines in the various CNS regions.

166 (RAGE), p-ERK1/2, nuclear NF-kappaB p65, and proinflammatory cytokines in vivo and in vitro.

167 ation inhibitory factor (MIF), a pleiotropic proinflammatory cytokine, in this process.

168 k of suppression of cytotoxic mediators, and proinflammatory cytokines, in peripheral blood T, NKT-li

169 in impaired induction of a broad spectrum of proinflammatory cytokines, including IL-1, IL-36, and th

170 , P2X7R activation induces the production of proinflammatory cytokines, including IL-1beta and IL-18,

171 crobial and stress products to activation of proinflammatory cytokines, including IL-1beta The potent

172 istently resulted in increased production of proinflammatory cytokines, including iNOS, TNF-alpha, an

173 the dysregulation of osteoclast activity by proinflammatory cytokines, including TNF, interferes wit

174 tivation characterized by elevated levels of proinflammatory cytokines, including type I interferons

175 Cellular stress and proinflammatory cytokines induce phosphorylation of insu

176 ar pattern by counteracting the synthesis of proinflammatory cytokines, inhibiting neutrophil traffic

177 These results suggest that proinflammatory cytokines interfere with oral tolerance

178 The proinflammatory cytokine interferon-gamma-induced protei

179 Increased level of proinflammatory cytokine interleukin (IL)-12 correlates

180 Basal tear levels of the proinflammatory cytokine interleukin 17A were significan

181 tivation, inducing maturation and release of proinflammatory cytokine interleukin-1beta (IL-1beta) an

182 ome promotes caspase-1-mediated secretion of proinflammatory cytokines interleukin (IL)-1beta and IL-

183 e Langerhans cell chemoattractant CCL20, and proinflammatory cytokines interleukin 1alpha (IL-1alpha)

184 , and quantitative RT-PCR (qRT-PCR), and the proinflammatory cytokines interleukin 1beta, interferon

185 T cells have emerged as major sources of the proinflammatory cytokines interleukin-17 (IL-17) and int

186 dent subjects compared with controls for the proinflammatory cytokines interleukin-6 and interleukin-

187 ntigen 4, anti-programmed death ligand 1) or proinflammatory cytokines (interleukin [IL] 12) were use

188 C-treated hearts show enhanced production of proinflammatory cytokines (interleukin-3, interleukin-6,

189 1 [MMP-1] and heme oxygenase 1 [HO-1]), and proinflammatory cytokines (interleukin-6 [IL-6], IL-8, m

190 xtra-respiratory organs in the production of proinflammatory cytokines is unknown.

191 Interleukin-1 (IL-1), an important proinflammatory cytokine, is suspected to play a role in

192 There were corresponding increased levels of proinflammatory cytokines KC (P = .0001) and IL-6 (P = .

193 Proinflammatory cytokines, keratinocyte chemoattractant

194 educed islet interleukin-1beta expression, a proinflammatory cytokine known to stimulate prostaglandi

195 e microglia could be ineffective and produce proinflammatory cytokines leading to progressive neurona

196 influx of astrocytes and microglia releasing proinflammatory cytokines leads to dramatic inflammation

197 ess-induced elevations in corticosterone and proinflammatory cytokine levels and depression-like and

198 duced inflammation, as measured by decreased proinflammatory cytokine levels and neutrophil recruitme

199 The classifier was also related to proinflammatory cytokine levels in serum (p=0.038).

200 decreased joint inflammation, swelling, and proinflammatory cytokine levels relative to WT mice.

201 Proinflammatory cytokine levels were increased in the se

202 king nanoparticles, termed MPhi-NPs, reduced proinflammatory cytokine levels, inhibited bacterial dis

203 at wild type mice had significantly elevated proinflammatory cytokine levels, reduced ejection fracti

204 Proinflammatory cytokines like TNFalpha cooperated with

205 ing and cellular activation by virus-induced proinflammatory cytokines like tumor necrosis factor and

206 with pH1N1/NSs-6mut induced lower levels of proinflammatory cytokines, likely due to a general inhib

207 IL-18 is a proinflammatory cytokine made upon activation of the inf

208 The elevated levels of this proinflammatory cytokine may explain the increased incid

209 xpression of the proapoptotic factor Bim and proinflammatory cytokines MCP-1, IL-6, and E-selectin.

210 Furthermore, as the primary source of proinflammatory cytokines, microglia are pivotal mediato

211 r (NF)-kappaB, which induced expression of a proinflammatory cytokine module that, along with the ant

212 Strategies to reduce levels of proinflammatory cytokines more broadly and increase anti

213 ifibrotic activity and reduced production of proinflammatory cytokines most likely by activation of t

214 LPS-induced P2X currents and proinflammatory cytokine mRNA expression were blocked by

215 A-sequencing analysis showed upregulation of proinflammatory cytokines, NF-kappaB signaling, and heat

216 Proinflammatory cytokine overproduction and excessive ce

217 ht bacterial infection, heightened levels of proinflammatory cytokines, overt granulocyte/monocyte pr

218 hagy and recapitulates the uric acid-induced proinflammatory cytokine phenotype.

219 ant to the inflammatory settings where these proinflammatory cytokines play a critical role.

220 IL-17A is a proinflammatory cytokine produced by diverse cell types,

221 iologics are currently available that target proinflammatory cytokines produced by T lymphocytes, but

222 heir ability to make IL-17, were more potent proinflammatory cytokine producers, and were powerful in

223 WT mice showed higher frequencies of proinflammatory cytokine-producing and lower frequencies

224 p38 mitogen-activated protein kinase-related proinflammatory cytokine production (P < .0007).

225 ific PRMT1 knock-out mice demonstrate higher proinflammatory cytokine production and a lower survival

226 ng trauma but displayed decreased stimulated proinflammatory cytokine production and significantly re

227 d survival, attenuated hypothermia, and less proinflammatory cytokine production during septic shock

228 S stimulated NF-kappaB activation and caused proinflammatory cytokine production in alveolar macropha

229 of Fas-mediated apoptosis and its effect on proinflammatory cytokine production in early alcoholic l

230 RGS10 has emerged as a key regulator of proinflammatory cytokine production in microglia, functi

231 Moreover, they were seen to stimulate proinflammatory cytokine production in primary human and

232 cally re-establishes normal homeostasis, and proinflammatory cytokine production returns to baseline.

233 Here, we report that ExoY inhibits proinflammatory cytokine production through suppressing

234 ent mice indicated that Acanthamoeba-induced proinflammatory cytokine production was through MyD88-de

235 these mice displayed enhanced proliferation, proinflammatory cytokine production, and effector molecu

236 mmaT and suppressing Th17 lineage stability, proinflammatory cytokine production, and pathogenicity.

237 successfully dampened PMA-induced ear edema, proinflammatory cytokine production, reactive oxygen and

238 duced NF-kappaB translocation and downstream proinflammatory cytokine production.

239 feration, differentiation, and migration and proinflammatory cytokine production.

240 ylation of Akt, which leads to a decrease in proinflammatory cytokine production.

241 ells promotes enhanced T cell activation and proinflammatory cytokine production.

242 ted with GC storage, tissue inflammation and proinflammatory cytokine production.

243 This was accompanied by an exaggerated proinflammatory cytokine profile and increased STAT3 sig

244 represents an efficacious and, based on its proinflammatory cytokine profile, targeted treatment opt

245 C) significantly reduced plasma LPS-elicited proinflammatory cytokines, reflecting endotoxin toleranc

246 ulum of tumor cells by triggering macrophage proinflammatory cytokine release after phosphatidylserin

247 downregulated markers of toxicity, including proinflammatory cytokine release and cellular proliferat

248 Proinflammatory cytokine release was determined after 2,

249 mula did not induce T-cell proliferation and proinflammatory cytokine release.

250 l4/del4) cholangiocytes, in turn, respond to proinflammatory cytokines released by macrophages by up-

251 lysaccharide to reduce the endotoxin-induced proinflammatory cytokine response in macrophages.

252 A proinflammatory cytokine response is associated with gre

253 in D3 resulted in an enhanced broad-spectrum proinflammatory cytokine response of cord blood mononucl

254 , and expansion of blood monocytes with less proinflammatory cytokine response to bacterial stimulati

255 Furthermore, BCD attenuated the CC-induced proinflammatory cytokine responses (e.g., IL-1alpha, MIP

256 ntrolling parasite burden by contributing to proinflammatory cytokine responses by DCs and natural ki

257 interferon (IFN), IFN-stimulating gene, and proinflammatory cytokine responses in Mavs(-/-) dendriti

258 ges (pH1N1/NSs-6mut) induced lower levels of proinflammatory cytokines, resulting in viral attenuatio

259 nhancement of cryptic peptides was caused by proinflammatory cytokines, secreted in response to micro

260 e, IL-26 allows extracellular DNA to trigger proinflammatory cytokine secretion by monocytes, in a ST

261 on of epithelial integrity, and induction of proinflammatory cytokine secretion by S. Paratyphi A but

262 a serovar Typhimurium-induced pyroptosis and proinflammatory cytokine secretion in macrophages.

263 e degrading desmosomal proteins and inducing proinflammatory cytokine secretion through protease-acti

264 66b(bright), CD63(bright) surface phenotype, proinflammatory cytokine secretion, and cytotoxicity.

265 FlaA:Betv1-mediated IL-10 secretion, but not proinflammatory cytokine secretion, was inhibited by rap

266 y through a mechanism dependent on NF-kappaB proinflammatory cytokine signaling pathway in both norma

267 F-kappaB activation following treatment with proinflammatory cytokines, specifically interleukin-1bet

268 erived from donor lungs, and not circulating proinflammatory cytokines substantially impaired the qua

269 cer cells in vitro induced the expression of proinflammatory cytokines such as CXCL5 by activating St

270 xicity against susceptible cells and secrete proinflammatory cytokines such as IFN-gamma.

271 1/IRAK-4-mediated signaling and secretion of proinflammatory cytokines such as IL-12, IL-6, or TNF-al

272 stitutive proteasomes after cell exposure to proinflammatory cytokines such as interferon-gamma.

273 exposure showed decreased gene expression of proinflammatory cytokines such as tumor necrosis factor-

274 gnificantly higher expression and release of proinflammatory cytokines, such as chemokine (C-C motif)

275 ctivation of caspase-1 and the maturation of proinflammatory cytokines, such as IL-1beta and IL-18.

276 ates inflammation by degrading mRNA encoding proinflammatory cytokines, such as IL6, IL1, and IL12.

277 +) monocytes, as well as increased levels of proinflammatory cytokines, such as TNF-alpha and IL-17.

278 ading to cell type-specific amplification of proinflammatory cytokines, such as TNF-alpha, IL-1beta,

279 h covR-deficient S. agalactiae produced less proinflammatory cytokines than those infected with wild-

280 IL-6 is a pleiotropic proinflammatory cytokine that is elevated in serum and s

281 eptor (TLR) 4, which leads to the release of proinflammatory cytokines that are essential for a poten

282 eptor-modified T cells (CAR T cells) produce proinflammatory cytokines that increase expression of T-

283 nalysis of human macrophages showed that the proinflammatory cytokines TNF and type I interferons ind

284 on of the NF-kappaB pathway and secretion of proinflammatory cytokines TNF-alpha and IL-6.

285 ition, CD70(-/-) hosts have higher levels of proinflammatory cytokines TNF-alpha, IFN-gamma, IL-2, an

286 atory protein cyclooxygenase (COX)-2 and the proinflammatory cytokines TNF-alpha, IL-6, and IL-12.

287 In this work, we titered bacteria and/or the proinflammatory cytokine TNFalpha in a set of establishe

288 An increase in proinflammatory cytokines (TNFalpha and KC/GRO) was obse

289 utes to their extraordinary vulnerability to proinflammatory cytokine toxicity and may therefore repr

290 ular barrier was impaired by Ca2+ depletion, proinflammatory cytokine tumor necrosis factor alpha, or

291 inked to the expression of the M1-associated proinflammatory cytokine tumor necrosis factor, inducibl

292 microglia in the ARC, the expression of the proinflammatory cytokine tumor necrosis factor-alpha in

293 Kal directly activated monocytes to produce proinflammatory cytokines, up-regulated their C5aR and F

294 oxin preconditioning reduced serum levels of proinflammatory cytokines, upregulated molecular pathway

295 ults together suggest that NRTIs up-regulate proinflammatory cytokines via a Wnt5a signaling-dependen

296 Paradoxically, IL-32, a proinflammatory cytokine, was lower in subpopulations of

297 in Ld-infected cells curtails production of proinflammatory cytokines, which are otherwise detriment

298 itantly, S. aureus elicits the production of proinflammatory cytokines, which could ultimately pertur

299 s significant inhibition in the synthesis of proinflammatory cytokines with a concordant blockade of

300 T2D, and these cells are the main source of proinflammatory cytokines within islets.