ライフサイエンスコーパス: cytokine production

1 mage is largely attributable to inflammatory cytokine production.

2 T cells and in general downregulated T cell cytokine production.

3 diversity, is associated with increased FGT cytokine production.

4 s, telomere maintenance, cell senescence and cytokine production.

5 mechanisms such as antigen presentation and cytokine production.

6 is, NFkappaB activation, and proinflammatory cytokine production.

7 pletely prevents NE-induced pro-inflammatory cytokine production.

8 ay hyperreactivity (AHR) and driven by T(H)2 cytokine production.

9 in human DCs and increases pro-inflammatory cytokine production.

10 TNF secretion and dysregulated inflammatory cytokine production.

11 mmune response, and the vascular response to cytokine production.

12 -available drugs to synergistically modulate cytokine production.

13 ll memory phenotypes/responses and bystander cytokine production.

14 ation of platelet-neutrophil aggregates, and cytokine production.

15 hrough its effect on NF-kappaB signaling and cytokine production.

16 eased the risk for candidemia independent of cytokine production.

17 valuate as some isolates induced substantial cytokine production.

18 ells suppressed T(H)2 cell proliferation and cytokine production.

19 lp, class switching, antibody production and cytokine production.

20 city to induce dendritic cell maturation and cytokine production.

21 ing sustained immune activation and effector cytokine production.

22 ractions in the Th2 locus, leading to type 2 cytokine production.

23 ng role for distinct sets of plasma cells in cytokine production.

24 (bright) NK cell subset characterized by low cytokine production.

25 atrophy, polarization imbalance, and altered cytokine production.

26 tment and bacterial clearance, and decreased cytokine production.

27 ressed mTORC1 activation and proinflammatory cytokine production.

28 Foxp3+ Treg frequency and immune regulatory cytokine production.

29 cules, and they were polyfunctional based on cytokine production.

30 rget-specific Ca(2+)-flux, degranulation and cytokine production.

31 location, which is critical for inflammatory cytokine production.

32 d IL-13 while TGF-beta had no effect on ILC2 cytokine production.

33 2 (LAMP2) and HIF-1alpha levels and modified cytokine production.

34 controls, as well as lymphocyte capacity for cytokine production.

35 -1 infection and HIV-stimulated inflammatory cytokine production.

36 iveness to factors that stimulate epithelial cytokine production.

37 of glucose uptake, glycolytic metabolism, or cytokine production.

38 and prevented termination of proinflammatory cytokine production.

39 peripheral red cell counts as well as normal cytokine production.

40 ncluding antigen presentation to T cells and cytokine production.

41 ) wounds demonstrated decreased inflammatory cytokine production.

42 phagocytic ability but have little effect on cytokine production.

43 nfected cells through cytotoxicity and rapid cytokine production.

44 nfectious burden, immune cell abundance, and cytokine production.

45 n primary T cells decreased Ca(2+) entry and cytokine production.

46 bosis, mucous secretions in the airways, and cytokine production.

47 ytometry and antigen specificity by in vitro cytokine production.

48 ow that rolipram increases anti-inflammatory cytokine production.

49 endent NF-kappaB activation and inflammatory cytokine production.

50 lating the sigma-1 receptor, which regulates cytokine production.

51 lec2d did not stimulate kinase activation or cytokine production.

52 with subsequent immune cell infiltration and cytokine production.

53 not monophosphoryl lipid A, pro-inflammatory cytokine production.

54 is considered important for proinflammatory cytokine production.

55 els emerge from differences in the levels of cytokine production.

56 gnalling pathways that mediate IL-33 induced cytokine production, a culture system was set up to obta

57 e-mediated inflammation and pro-inflammatory cytokine production, a shift towards ketone bodies as th

58 In addition to cytokine production, acute mast cell degranulation is a

59 the role of the MK2/3/TTP signaling axis in cytokine production also in vivo.

60 cy comparable to that of Cas9 CAR-T cells in cytokine production and cancer cell killing, while expre

61 milar between the co-cultures (cytotoxicity, cytokine production and caspase activity).

62 ia, however, glycolysis becomes critical for cytokine production and cell survival.

63 cin targets p70S6K and 4EBP1, with decreased cytokine production and cellular proliferation and incre

64 TCRs mediate enhanced T cell proliferation, cytokine production and cytotoxicity, while reducing the

65 apidly respond to antigenic stimulation with cytokine production and direct cytotoxicity.

66 ost capacity for Toll-like-receptor-mediated cytokine production and do not induce T cell activation,

67 Cellular responses were characterized by cytokine production and flow cytometry, and in a subset

68 Cellular responses were characterised by cytokine production and flow cytometry, and in a subset

69 umerous functions including gene expression, cytokine production and gliotransmitter release.

70 sic metabolic pathways controlling MAIT cell cytokine production and highlight mTORC1 as an important

71 cells (CRTH2) receptor axis potently induces cytokine production and ILC2 migration.

72 ss of progenitor cells, leading to increased cytokine production and increased stem cell proliferatio

73 inhibition of STAT6 activation downregulates cytokine production and induces cell-cycle arrest in MF/

74 s CD4(+) T cell differentiation and effector cytokine production and may play a role in augmenting or

75 ed evidence of rapid activation and enhanced cytokine production and mediated protection after brain

76 N-alpha inhibited Toll-like receptor-induced cytokine production and monocyte-induced T-cell prolifer

77 azone elicited similar changes in macrophage cytokine production and neutrophil migration as exogenou

78 LA significantly suppressed LPS-induced cytokine production and NF-kappaB transcriptional activi

79 imulated PBMCs resulted in reduction of both cytokine production and phosphorylated Akt.

80 GRP potently inhibited alarmin-driven type 2 cytokine production and proliferation by lung ILC2s both

81 emphasis on recent work on the regulation of cytokine production and proliferation.

82 M also significantly reduced proinflammatory cytokine production and release following transplantatio

83 tb LAM did elicit pro- and anti-inflammatory cytokine production and release in a TLR2/1-dependent ma

84 we report that encounters with FRCs enhanced cytokine production and remodeled chromatin accessibilit

85 s exhibited impaired influenza virus-induced cytokine production and revealed that IRF5 acts downstre

86 D169(+) moDCs and Axl(+) CD169(+) DCs led to cytokine production and robust cross-presentation and ac

87 Allergen-specific antibodies, splenocyte cytokine production and splenic forkhead box P3 (FOXP3)(

88 Specifically, the impact of HCQ on cytokine production and suppression of antigen presentat

89 CD4(+) T-cell extrinsic, whereas changes in cytokine production and T(FH) cell function were cell in

90 rted treatment, IFN-alpha inhibited monocyte cytokine production and T-cell stimulation ex vivo.

91 tion is directly linked to both inflammatory cytokine production and Toll-like receptor (TLR) express

92 trol infection fail to do so due to impaired cytokine production and/cytotoxic effector cell function

93 of tolerogenic cytokines, inhibition of Th2 cytokines production and a modulation of oxidative stres

94 sponse, mediating 1) IgE-dependent mast cell cytokine production, and 2) histamine-induced endothelia

95 NK cell activation, degranulation, chemokine/cytokine production, and Ab-dependent cellular cytotoxic

96 ally active enzymes, loss of proinflammatory cytokine production, and acquisition of novel driver mut

97 creases allergen-induced IL-33 release, ILC2 cytokine production, and airway inflammation.

98 reduce parasite burden through phagocytosis, cytokine production, and antigen presentation.

99 Leukocyte recruitment, cytokine production, and bacterial clearance were measur

100 We measured cytotoxicity, cytokine production, and bacterial growth, following api

101 Necrosome signaling, cytokine production, and cell death were evaluated by im

102 l-spleen tryptophan metabolism, inflammatory cytokine production, and cognitive decline; and they pro

103 s histologic damage, reduced proinflammatory cytokine production, and diminished production of reacti

104 eceptor and transcription factor expression, cytokine production, and gene expression with flow cytom

105 ng antibody secretion, antigen presentation, cytokine production, and generation of immunological mem

106 and analyzed the microbiomes, chemokine and cytokine production, and immune cells and transcriptomes

107 wed increased permeability, pro-inflammatory cytokine production, and increased oxidative stress.

108 pram inhibits organ damage, pro-inflammatory cytokine production, and intracellular migration of earl

109 ecule retinoic acid, inhibiting inflammatory cytokine production, and making macrophages more suscept

110 ency increased phagocytosis, proinflammatory cytokine production, and netosis in neutrophils, thereby

111 evaluated for expression of surface markers, cytokine production, and proliferation of Th2 as well as

112 results in reduced proliferation, decreased cytokine production, and reduced expression of many lymp

113 on of multiple inhibitory receptors, limited cytokine production, and reduced proliferative capacity.

114 lation was supported by the immune profiles, cytokine production, and results of the TCR repertoire a

115 ed that DHX37 suppresses effector functions, cytokine production, and T cell activation.

116 cell-cell contact, antigen presentation, and cytokine production, and thereby participate in systemic

117 iferative programs, promoting proliferation, cytokine production, and tissue invasion.

118 burden, to prevent lung damage, to modulate cytokine production, and to improve host survival.

119 activation, inhibiting their proliferation, cytokine production, and tumor killing capacity.

120 defenses coupled with exuberant inflammatory cytokine production are the defining and driving feature

121 g pathway to induce immune-suppressive IL-10 cytokine production as a means to dampen the host defenc

122 1B-induced inflammation in A549 cells, using cytokine production as outputs and testing effects of OR

123 ic smooth muscle cell-dependent inflammatory cytokine production as well as decreases neutrophil tran

124 rved increased ILC2 proliferation and type 2 cytokine production as well as exaggerated responses to

125 gut microbiota composition and inflammatory cytokines production associated with acute and chronic i

126 s from IL-10-neutralized animals had reduced cytokine production but increased fibrosis relative to c

127 HDM also induced proinflammatory cytokine production, but reduced granulocyte recruitment

128 acellular pathways are activated, initiating cytokine production, but these pathways are incompletely

129 Cytokine production by antigen-presenting cells and othe

130 We sought to measure cytokine production by circulating skin-homing (CLA(+))

131 Type 2 cytokine production by CRTH2(-)IL7Ralpha(-) innate lymph

132 upregulation of DUSP4, leading to imbalanced cytokine production by effector T cells.

133 ated anticardiolipin stimulates inflammatory cytokine production by endothelial cells and a trophobla

134 All lactobacilli induced inflammatory cytokine production by genital epithelial cells and prod

135 inhibits host translation, thereby impairing cytokine production by infected macrophages.

136 ion of proinflammatory and anti-inflammatory cytokine production by macrophages.

137 2-DG inhibits proinflammatory cytokine production by MDM and monocyte-derived dendriti

138 IFN-beta did not induce inflammatory cytokine production by MDMs or PBECs but reduced influen

139 /2-MyD88-NF-kappaB-dependent proinflammatory cytokine production by monocytes and macrophages of huma

140 on myeloid cells and induce proinflammatory cytokine production by monocytes and NETosis by neutroph

141 significantly higher levels of chemokine and cytokine production by NLRC5(-/-) THP-1 macrophages than

142 Cytokine production by peripheral blood mononuclear cell

143 (hi) cells, suppressed the proliferation and cytokine production by stimulated CD4(+) T cells.

144 cerebrum and spleen, including inflammatory cytokine production by stimulated splenocytes, from fema

145 enhance tumor growth through suppression of cytokine production by tumor-infiltrating CD8(+) T cells

146 Cytokine production by vaginal epithelial cells in respo

147 t also NK cells, displayed reduced antiviral cytokine production capability.

148 Cytokine production capacity after ex vivo stimulation o

149 y morning vaccination resulted in a superior cytokine production capacity compared with later morning

150 ells localized inside tumors, with increased cytokine production capacity.

151 ng those genes involving in immune response, cytokine production, cell proliferation and apoptosis.

152 ositive monocytes and a lack of inflammatory cytokine production compared to mice inoculated with con

153 A cohort of septic patients had increased cytokine production compared with controls consistent wi

154 s displayed increased NF-kappaB activity and cytokine production compared with the cells isolated fro

155 stress and ensuing placental senescence and cytokine production could represent a broad theme in emb

156 verge into distinct subsets, which differ in cytokine production, cytotoxicity, homing, and memory tr

157 e degree of hyperferritinemia and pattern of cytokine production differed between MIS-C and MAS.

158 gen-dependent signals in NKT cells to dampen cytokine production during early innate immune activatio

159 as a regulator of myeloid cell inflammatory cytokine production during IAV infection in mice and hum

160 for NF-kappaB activation and proinflammatory cytokine production during infection.

161 ng and inhibitory events that evoked diverse cytokine production dynamics.

162 e largely driven by the environment, whereas cytokine production elicited by microbial antigens was m

163 ter 1 (Glut1) expression for proinflammatory cytokine production, especially IL-1beta.

164 itor, on endotoxin-inducible proinflammatory cytokine production ex vivo in whole blood of patients w

165 opria lymphocyte (LPL) activation status and cytokine production (flow cytometry), cytokine mRNA and

166 CD154 expression and cytokine production following Ag exposure compared with

167 sion using lentivirus infection dampened the cytokine production following bacterial challenge throug

168 T1(PD/PD) mast cells are equally impaired in cytokine production following FcepsilonRI stimulation, i

169 peritonsillar abscess (PTA) by analyzing the cytokine production following T cell receptor (TCR) and

170 Infection increased cytokine production from gastric epithelial cells and ma

171 Ligands for FFAR3 induced Th2 cytokine production from human and murine T cells, inclu

172 ntrol probe (S)-DO271, augments inflammatory cytokine production from human THP-1 macrophage cells.

173 This yeast elicits strong inflammatory cytokine production from innate cells harboring the IBD-

174 a significant effect on T-helper lymphocyte cytokine production >1 year later.

175 del for how these steps collectively control cytokine production has not been established.

176 he B cell effector functions of antibody and cytokine production, high expression of inhibitory recep

177 iciently upregulating activation markers and cytokine production, IAV-induced CCR5 downregulation was

178 erved in regard to lymphoblast expansion and cytokine production (IFN-gamma, IL-2, and TNF), with the

179 key in allergic asthma and regulates type 2 cytokine production, IgE secretion, and airway hyperresp

180 re performed, and airway eosinophilia, T(H)2 cytokine production, immunoglobulin synthesis, airway re

181 rdinated reduction in spleen proinflammatory cytokine production in 17-month-old mice.

182 IRAK4-MyD88 interactions and IRAK4-mediated cytokine production in a cysteine 13-dependent manner.

183 te and adaptive immune responses, and type 2 cytokine production in a model of airway sensitization a

184 sponse metabolite succinate and inflammatory cytokine production in a model of LPS-induced inflammati

185 infiltration, collagen accumulation, and Th2 cytokine production in allergic airways.

186 d TNF-alpha, and stimulate proliferation and cytokine production in allogeneic CD4(+) and CD8(+) T ce

187 into phosphatidic acid, limits inflammatory cytokine production in an arthritic mouse model dependen

188 ced the LPS-induced TAK1 phosphorylation and cytokine production in bone marrow-derived macrophages.

189 lper T (T(FH)) cells and dramatic changes in cytokine production in both patients and mice.

190 iciencies, RSV poorly induced maturation and cytokine production in CB and AB mDC.

191 t binds Lck to elicit signals that result in cytokine production in CD4(+) T effector cells (Teff).

192 orks that define the magnitude and timing of cytokine production in CD8(+) T cells.

193 after transplantation drive proinflammatory cytokine production in conventional T cells (Tconv) and

194 ne dinucleotide concentrations and impairing cytokine production in differentiating T cells.

195 mune complex deposition, and modulate TLR7/9 cytokine production in female MRL/lpr mice.

196 ed oxidative burst in human neutrophils, and cytokine production in human peripheral blood mononuclea

197 was less thoracic inflammation and increased cytokine production in lung granulomas and lymph nodes f

198 ogy, leukocyte recruitment, and inflammatory cytokine production in lungs including TNF, IL-6, IL-10,

199 heme-induced ROS, MAPK phosphorylation, and cytokine production in macrophages.

200 statins from increasing Rac1 GTP-loading and cytokine production in macrophages.

201 uitin proteome also enhanced proinflammatory cytokine production in mice stimulated with a sub-lethal

202 ystemic inflammation, a dramatic decrease of cytokine production in MK2/3 DKO, TTPaa, and DKO/TTPaa m

203 We compared TTP expression and cytokine production in mouse bone marrow-derived macroph

204 ed anti-fungal signaling and proinflammatory cytokine production in myeloid cells.

205 Because of cytokine production in nonhematopoietic tissues, the pot

206 glycolytic reprogramming for proinflammatory cytokine production in normoxia is not obvious, and effe

207 in mouse bone marrow-derived mast cells and cytokine production in peritoneal mast cells.

208 dly prevented IgE-mediated degranulation and cytokine production in primary human mast cells and bloc

209 responsive and competent for antigen-induced cytokine production in RAT and PTA.

210 gly, GM-CSF signaling amplifies inflammatory cytokine production in recruited monocytes by enhancing

211 % of the susceptibility loci affect in vitro cytokine production in response to Candida.

212 In vitro, Notch inhibition limited basophil cytokine production in response to cytokine stimulation.

213 ed to a decrease in T cell proliferation and cytokine production in response to IFX aggregates.

214 ected 30 d postvaccination showed heightened cytokine production in response to IL-15 compared with P

215 rotein in negatively regulating inflammatory cytokine production in response to interleukin-1beta (IL

216 ed eosinophilic lung inflammation and type 2 cytokine production in response to subsequent Df challen

217 ellular decision to initiate proinflammatory cytokine production in response to TLR activation.

218 dic acid axis as a modulator of inflammatory cytokine production in sJIA and CSS.

219 leotide cGAMP, a second messenger initiating cytokine production in subsets of myeloid lineage cell t

220 d degranulation assay, calcium mobilization, cytokine production in supernatants, assessment of viabi

221 ligands potently lower the Ag threshold for cytokine production in T cells.

222 stimulation by CD28, CD2, and CD27 increased cytokine production in this system, the Ag threshold rem

223 nts of wheat flour selectively induce type 2 cytokines production in baker's rhinitis.

224 (ROS) generation, transcription factor, and cytokines production in human gingival fibroblast cells

225 ties of inhibiting multiple pro-inflammatory cytokines production in macrophages and toxin-induced in

226 In vitro, CMP-001 induced cytokine production, including IFN-alpha from plasmacyto

227 on innate immune-associated proinflammatory cytokine production, including IL-1beta and IL-6.

228 flammation, goblet cell hyperplasia, and Th2 cytokine production, including IL-4, IL-5, and IL-13.

229 type I IFN-dependent decline in inflammatory cytokine production, independent of IL-10, whereas infla

230 hrough pattern-recognition receptor-mediated cytokine production, inflammasome activation, and apopto

231 While GPX4 does not control AA metabolism, cytokine production is governed by similar mechanisms as

232 dition, we identified that subclass-specific cytokine production is orchestrated at the posttranscrip

233 In the non-pathogenic setting, their cytokine production is regulated by serum amyloid A prot

234 To determine how activated ILC cytokine production is regulated, ILC subsets were activ

235 lar leakage can be reduced without impairing cytokine production, leukocyte recruitment, and pathogen

236 pecies production and inflammatory chemokine/cytokine production may contribute to tissue injury at t

237 n T-cell proliferation (P = .001), and T(H)2 cytokine production mediated by primed dendritic cells.

238 dependent cellular cytotoxicity, CD4+ T-cell cytokine production, memory B cell (MBC) activation, and

239 cific T cell receptors (TCRs) show increased cytokine production, migration toward tumor cells, and t

240 Both VNP versions induced proliferation and cytokine production of allergen-specific T cells in vitr

241 ed directly to cytotoxicity and inflammatory cytokine production of bone marrow-derived macrophages f

242 presence of IL-10 had a marked reduction in cytokine production of IL-5 and IL-13 while TGF-beta had

243 development, recruitment, localization, and cytokine production of immune and epithelial effector ce

244 rating lymphocytes in AIH, we determined the cytokine production of infiltrating cells obtained from

245 imited metabolic activity, proliferation and cytokine production of Th17 cells in BALB/c mice was ass

246 not simultaneously regulate pro-inflammatory cytokine production, oxidative stress, and recruitment o

247 urface proteins that bind IgG and facilitate cytokine production, phagocytosis, and Ab-dependent, cel

248 Analysis of their cytokine production profiles and transcriptome revealed

249 o DEPs, leading to increased proinflammatory cytokine production, reduced phagocytic function of alve

250 role of ROS in proinflammatory signaling and cytokine production remains unknown.

251 Macrophage-mediated phagocytosis and cytokine production represent the front lines of resista

252 These Trm populations exhibited distinct cytokine production, secondary memory potential, and tra

253 y inflammation and significantly reduced Th2 cytokine production, serum IgE levels, and airway hyperr

254 immune pathology and associated inflammatory cytokine production, specifically reducing cytokine-prod

255 creased effect of LPS on NOS2 expression and cytokine production, suggesting that O-GlcNAcylation may

256 lactic acid and induced greater inflammatory cytokine production than those from women with optimal m

257 anage the metabolically expensive process of cytokine production that drives relapse in those tumors

258 binding protein 1 (N4BP1) as a suppressor of cytokine production that is cleaved and inactivated by c

259 has been linked to enhanced proinflammatory cytokine production that promotes a Th2-type immune envi

260 d molecular pattern, inducing TLR4-dependent cytokine production through the MyD88 pathway, independe

261 ndency led to impaired homeostasis and T(H)2 cytokine production, thus inhibiting the development of

262 viability within macrophages, and decreased cytokine production (TNF-alpha, IL-1beta) at both mRNA a

263 lpha (P < 0.03), and reduced proinflammatory cytokine production (TNF-alpha, P < 0.04; IL-1beta, P <

264 a switch from predominantly proinflammatory cytokine production to chemokine production is a key fea

265 ession in DC enhances proinflammatory innate cytokine production to promote an altered Th2 immune res

266 d with GSK J4 altered coactivation of T cell cytokine production to RSV as well as a primary OVA resp

267 nd effector Th2 cells, confinement of type 2 cytokine production to the CD4+ effector population, a h

268 elective C5aR2 activation also downregulated cytokine production triggered by various TLRs (TLR2, TLR

269 ons, only marginally affects proinflammatory cytokine production triggered through NOD1 or TLR4.

270 sms regulating prolonged ILC2-mediated T(H)2 cytokine production under chronic inflammatory condition

271 Cementoblast cytokine production under different treatment conditions

272 heir recognition of glycolipid Ags and rapid cytokine production upon activation.

273 We assessed cytokine production via enzyme-linked immunosorbent assa

274 ecovery of antigen-specific and non-specific cytokine production via metformin-mediated increase in g

275 Cytokine production was assessed after 24 hours, 48 hour

276 mes was studied by qPCR and western blot and cytokine production was assessed by multiplex assays.

277 Cytokine production was assessed by quantitative polymer

278 Furthermore, patient C. albicans-induced cytokine production was influenced by two human CD82 sin

279 Cytokine production was measured to assess the induction

280 Cytokine production was measured using flow cytometry, e

281 Cytokine production was measured using flow cytometry, E

282 Ag-reactive CD4 cytokine production was restricted to CD4 cells with an

283 Allergen-specific T-cell proliferation and cytokine production was significantly exacerbated by ATI

284 After 2 h of EVLP, cytokines production was significantly increased (IL-1be

285 To investigate how TLR triggering supports cytokine production, we adapted the protocol for flow cy

286 flammation, goblet cell hyperplasia, and Th2 cytokine production were attenuated in WT mice that were

287 duction of reactive oxygen species (ROS) and cytokine production were evaluated.

288 No significant differences in cytokine production were found in Th1, Th2, and Th17 imm

289 s pollen-driven T(H)2 cell proliferation and cytokine production were measured by using tritiated thy

290 Allergen transport and cytokine production were measured.

291 l/fl) counterparts; the effects of DC on Th1 cytokine production were mediated through production of

292 differences in NK cell or ILC frequencies or cytokine production were seen between vaccinated and Ad-

293 a significant increase in degranulation and cytokine production when basophils are activated in the

294 -recruiting ITAM of CD3epsilon reduced CAR-T cytokine production whereas the basic residue rich seque

295 y RVVC showed an increased monocytes-derived cytokine production which might contribute to an exagger

296 from apoptosis and triggered proinflammatory cytokine production, which in IL-10-deficient mice was a

297 paB (NF-kappaB) signaling and contributes to cytokine production while inhibiting apoptosis.

298 d skin lesion formation and pro-inflammatory cytokine production, while increasing bacterial clearanc

299 nded with reduced virus-induced inflammatory cytokine production, with IRF5 acting downstream of Toll

300 )-, and FSK-induced IL-6 gene expression and cytokine production without affecting cAMP-mediated phos