ライフサイエンスコーパス: cytokine production

1 iminished Vdelta2(+) T cell pro-inflammatory cytokine production.

2 entiation, and migration and proinflammatory cytokine production.

3 ssion such as VIC activation or inflammatory cytokine production.

4 meability via CB1 (P < 0.0001) and decreased cytokine production.

5 ast cell differentiation, proliferation, and cytokine production.

6 to T cells re-activation and pro-atherogenic cytokine production.

7 nt by ligands triggering granule release and cytokine production.

8 ibited MRL.Fas(lpr) T cell proliferation and cytokine production.

9 activation and a predominant Th1 profile of cytokine production.

10 ng pathway that integrates cell survival and cytokine production.

11 which leads to a decrease in proinflammatory cytokine production.

12 s limited to CD4(+) T cell proliferation and cytokine production.

13 macrophages, and globally suppressed T-cell cytokine production.

14 rs both the number of ILC2 and their type II cytokine production.

15 monstrated through morphological changes and cytokine production.

16 in regulating neutrophilic inflammation and cytokine production.

17 ved therapies, inhibit T-cell activation and cytokine production.

18 ion was determined by proteomic analysis and cytokine production.

19 miRNAs markedly reduced cardiac RNA-induced cytokine production.

20 associated with increased NF-kappaB-mediated cytokine production.

21 , as well as splenic T-helper-2 cell-derived cytokine production.

22 tive phosphorylation (OXPHOS) for energy and cytokine production.

23 ontrols with regard to iNKT-TCR affinity and cytokine production.

24 ntigen-specific proliferative responses, and cytokine production.

25 ion suppressed TIL expansion and altered TIL cytokine production.

26 erturb this response, resulting in decreased cytokine production.

27 functions: degranulation, cytotoxicity, and cytokine production.

28 eir survival, proliferation, activation, and cytokine production.

29 ivity, leading to increased calcium flux and cytokine production.

30 from C3-deficient mice did not show impaired cytokine production.

31 is mediated through direct cytotoxicity and cytokine production.

32 on in neonatal liver, resulting in increased cytokine production.

33 e accuracy of subset enrichment by measuring cytokine production.

34 55-3p, abolished LA effects on IL-33-induced cytokine production.

35 sponse to dysregulated local proinflammatory cytokine production.

36 g cell proliferation, maturation markers and cytokine production.

37 ggesting that the centrosome is critical for cytokine production.

38 he CNS and attenuated Th1/Th17 cell-mediated cytokine production.

39 ctivation of kidney-infiltrating T cells and cytokine production.

40 d RIG-I-like receptor-dependent inflammatory cytokine production.

41 l (APC) function in T-cell polarization, and cytokine production.

42 es p38 MAPK and SGK-1, resulting in Th2 cell cytokine production.

43 ular glucose metabolism and Borrelia-induced cytokine production.

44 which resulted in dampening of the excessive cytokine production.

45 hanced T cell activation and proinflammatory cytokine production.

46 ed facilitated allergen presentation and Th2 cytokine production.

47 cal regulators of inflammatory responses and cytokine production.

48 age, tissue inflammation and proinflammatory cytokine production.

49 stion manifest in impaired proliferation and cytokine production.

50 lular responses, including degranulation and cytokine production.

51 bal defect in the development of Ag-specific cytokine production.

52 l infiltrate and high levels of inflammatory cytokine production.

53 a maturation, lung cellular recruitment, and cytokine production.

54 al pathways while also limiting inflammatory cytokine production.

55 translocation and downstream proinflammatory cytokine production.

56 whereas CpG-ODN-primed mice showed augmented cytokine production.

57 o the intestine, and increasing inflammatory cytokine production.

58 ) mediates autoantigen and viral RNA-induced cytokine production.

59 on T cells capable of both proliferation and cytokine production after antigen restimulation was asse

60 ally, we found that Src inhibitors decreased cytokine production after coculture, indicating that Src

61 ent as well as prevents oxidative stress and cytokine production after MI.

62 CD4(+) T cell-proliferative response and TH2 cytokines production after casein stimulation in childre

63 h by sustained Ca(2+) influx or by enhancing cytokine production, aggravating inflammation and tissue

64 -out mice demonstrate higher proinflammatory cytokine production and a lower survival rate after ceca

65 d we investigated their role in DENV-induced cytokine production and adaptive immune responses.

66 c signal that promotes optimal innate immune cytokine production and antibacterial defense, demonstra

67 e-1 and NF-kappaB activation, Th1 polarizing cytokine production and autologous Th1 polarization.

68 s in other cholangiocytes including elevated cytokine production and cell proliferation.

69 netic host factors (e.g., age and gender) on cytokine production and circulating mediators.

70 ILC2s) resemble type 2 helper (Th2) cells in cytokine production and contribute to anti-helminth immu

71 In vivo experiments revealed that T-cell cytokine production and cutaneous recall responses were

72 l-like receptor 2, -4, and -9 expression and cytokine production and function were studied ex vivo at

73 RNA of both human and rodent origins induced cytokine production and immune cell activation.

74 functions of the immune system, most notably cytokine production and immune cell migration, are under

75 g pathway p38-CREB in DCs, thereby impairing cytokine production and in consequence T cell priming to

76 toid arthritis patients reduced inflammatory cytokine production and increased IL-10 production.

77 metabolic pathways with metformin diminished cytokine production and increased mortality in systemic

78 kinase TAK1 in monocytes blocked TLR-induced cytokine production and IRF5 translocation to the nucleu

79 Enhanced pro-inflammatory cytokine production and JNK activity under hypoxia were

80 rkat T cells, degranulated NK cells, induced cytokine production and killed Env-expressing cells.

81 tional inhibition of Dkk-1 impaired Th2 cell cytokine production and leukocyte infiltration, protecti

82 ators and that the miRNAs most likely induce cytokine production and leukocyte migration through TLR7

83 buting to IAV pathogenesis through increased cytokine production and lung cellular infiltrates.

84 that was coordinated with lipid mediator and cytokine production and lytic IEC death.

85 ory switch to control osteoclastogenesis and cytokine production and may be a control point underlyin

86 Moreover, glibenclamide reduced cytokine production and migration capacity of infected P

87 ed by diminished airway eosinophilia, type 2 cytokine production and mucus secretion after allergen i

88 mmunological experiments to measure in vitro cytokine production and neutrophil responses to a subset

89 es antitumor function, T-cell expansion, and cytokine production and preserves a central memory pheno

90 eting PI3Kdelta activity can modulate T-cell cytokine production and reduce inflammation in vivo, sug

91 splayed decreased stimulated proinflammatory cytokine production and significantly reduced human leuk

92 p3(Cre)xT-bet(fl/fl) mice revealed unaltered cytokine production and suppressive capacity.

93 ifferentiate through stages of localization, cytokine production and surface ligand expression to 'fi

94 sustained Ca(2+) signaling for inflammatory cytokine production and the killing of target cells; how

95 We further show that pDCs suppress cytokine production and the proliferation rate while inc

96 ubsets of CD4(+) T helper cells and assessed cytokine production and transcription factor expression.

97 in an antigen-dependent manner as judged by cytokine production and tumor killing, and redirected by

98 increased differentiation, reduced effector cytokine production, and a reduced reproliferative respo

99 accumulation of ILC2s and TH2 cells, type 2 cytokine production, and airway hyperresponsiveness comp

100 cid-base status, metabolism, organ function, cytokine production, and coagulation.

101 ayed enhanced proliferation, proinflammatory cytokine production, and effector molecule expression.

102 rate increased AHR, airway inflammation, TH2 cytokine production, and immunoglobulin levels and a mod

103 lyzed the killing activity, oxidative burst, cytokine production, and in vitro effects of rhIFN-gamma

104 mice display higher viral burdens, enhanced cytokine production, and increased mortality after influ

105 ative stress, increased interstitial sodium, cytokine production, and inflammasome activation promote

106 host myeloid cell counts, cell recruitment, cytokine production, and iron gene expression were deter

107 ay inflammation, allergic sensitization, TH2 cytokine production, and mucous cell metaplasia.

108 siological end points such as proliferation, cytokine production, and other responses to stimulation.

109 sing Th17 lineage stability, proinflammatory cytokine production, and pathogenicity.

110 tional characterization using degranulation, cytokine production, and proliferation assays.

111 an enhanced memory phenotype, have increased cytokine production, and provide protection against leth

112 y a shift in microglial phenotype, increased cytokine production, and reduced phagocytic capacity.

113 man B cells suppresses B cell proliferation, cytokine production, and signal transduction.

114 y molecule expression, limited TH-polarizing cytokine production, and significant cell death, BCG ind

115 FAT1, as well as reduced cell proliferation, cytokine production, and the antitumor activity of CD8(+

116 d by histamine together with mDCs phenotype, cytokine production, and the stimulatory and polarizing

117 rmine the mechanisms by which TL1A regulates cytokine production, and whether these associate with ou

118 tumor growth through direct growth-promoting cytokine production, angiogenesis, and ROS production.

119 infiltration of neutrophils and inflammatory cytokine production are impaired in M-ILK-deficient mice

120 he mechanisms by which glibenclamide affects cytokine production are unknown.

121 s associated with excessive pro-inflammatory cytokine production as well as an increase in acute tiss

122 T-cell receptor-driven calcium response and cytokine production associated with the loss of alpha2de

123 prisingly enhanced IgE-mediated protease and cytokine production both in vitro and in vivo.

124 aling cascade, thereby blocking inflammatory cytokine production but also inducing apoptosis.

125 d TCR engagement, costimulation, and priming cytokine production but are critical for the generation

126 ferentiated in vitro, ORAI1 was required for cytokine production but not the expression of Th1- and T

127 back had no effect on Th1- or Th17-signature cytokine production, but it promoted Th2- and Th9-associ

128 d fibroblasts activated IFN-gamma and IL-17A cytokine production by autologous, NTHi-specific lung CD

129 Dexamethasone inhibited type 2 cytokine production by blood ILC2s.

130 protein MyD88 were required for IAPP-induced cytokine production by BMDMs, a process that is partiall

131 novel molecular mechanism underlying type 2 cytokine production by CD8(+) T cells, revealing a more

132 inhibitory receptors differentially affected cytokine production by cells in response to staphylococc

133 nuation of inflammatory cell recruitment and cytokine production by dexamethasone impairs proliferati

134 e significant induction of proliferation and cytokine production by diabetogenic T cells.

135 Cytokine production by GC Tfh cells may be intrinsically

136 In addition, there is decreased cytokine production by Hdac3-deficient NKT2 and NKT17 ce

137 veal and begin to explain the variability in cytokine production by human immune cells in response to

138 NARE complexing is a key regulatory step for cytokine production by immune cells and prove the applic

139 the Yersinia virulence factor YopJ inhibits cytokine production by innate immune cells but also trig

140 coded by TIRAP) has appeared crucial for the cytokine production by Ly6C(lo) but not by Ly6C(hi) mono

141 T-cell receptor-driven calcium responses and cytokine production by mouse and human TH2 cells with no

142 h fibrosis values predicted strong antiviral cytokine production by NK cells.

143 ng parasite RBC invasion and proinflammatory cytokine production by parasite-stimulated monocytes in

144 Tregs to restrain proliferation and effector cytokine production by responders or through conversion

145 miR-24-TCF1 pathway in controlling effector cytokine production by T cells and further suggest miR-2

146 Cytokine production by T cells from peripheral lymph nod

147 Cytokine production by T cells from vaccinated subjects

148 C supernatant or control medium, after which cytokine production by T cells was determined.

149 Infection, phenotype, and cytokine production by T cells were analyzed by flow cyt

150 f adherent antigen-presenting cells modulate cytokine production by T cells.

151 STAT3 drives development of Th17 cells and cytokine production by Th2 and Th17 cells, which contrib

152 ight IL-2 as a critical component in optimal cytokine production by Th2 and Th9 cells in vitro and in

153 -presenting cells are immunogenic, promoting cytokine production by the cells in which they are forme

154 sation of tumor growth and partial rescue of cytokine production by the dysfunctional TILs, with only

155 that tumor-induced central pro-inflammatory cytokine production can exist in the absence of depressi

156 effect on NK cell functions, with increased cytokine-production capabilities following engagement of

157 e a strong impact of genetic heritability on cytokine production capacity after challenge with bacter

158 l cell AR signaling in mouse models promotes cytokine production cell-autonomously, impairs epithelia

159 on binding to its receptor, TNFR1, can drive cytokine production, cell survival, or cell death.

160 and decreased wound macrophage inflammatory cytokine production compared with control animals.

161 d a more activated phenotype (proliferation, cytokine production) compared with iTreg(-) In contrast

162 Increased cytokine production correlated with reduced degradation

163 pecies and found to induce similar levels of cytokine production despite being internalized by macrop

164 Candida spp. elicit cytokine production downstream of various pathogen recog

165 derate the pathological effects of excessive cytokine production during sepsis.

166 nuated hypothermia, and less proinflammatory cytokine production during septic shock caused by cecal

167 t they inhibit TNFalpha-induced inflammatory cytokine production (E-selectin, ICAM-1, VCAM-1 and IL-6

168 isition of an activated phenotype, increased cytokine production, enhanced proliferation, and a trans

169 s to modify TLR7/8- or RSV-stimulated innate cytokine production, even at supraphysiologic concentrat

170 d Vdelta2(+) counts, cellular phenotype, and cytokine production following in vitro stimulation at as

171 paired T-cell activation, proliferation, and cytokine production following polyclonal and antigen-spe

172 CDC42BPA, DTNBP1, FERMT2, PRKCZ, RAC1), and cytokine production (FOXP1, IRF8, MR1).

173 PAHSAs also reduce inflammatory cytokine production from immune cells and ameliorate adi

174 vity was measured by in vitro suppression of cytokine production from lipopolysaccharide-stimulated l

175 miR-183C expression enhanced pathogenic cytokine production from Th17 cells during their develop

176 peripheral blood or cerebrospinal fluid for cytokine production, gene expression, plasticity, homing

177 ng antigens and we found very little in vivo cytokine production, gross pathology or granuloma format

178 Interpretation: Pro-inflammatory cytokine production had a dose-dependent and temporal as

179 Immunological phenomena, including skewed cytokine production, have been observed among children w

180 own contributors to host immunity, including cytokine production, help for CD8(+) T and B cells, and

181 ) T cells that are characterized by impaired cytokine production, high coexpression of inhibitory rec

182 ing, histologic changes in inflammation, and cytokine production; however, FXII-deficient mice develo

183 triggered vigorous NK cell degranulation and cytokine production (i.e., TNF-alpha and IFN-gamma) agai

184 tumor microenvironment and angiogenesis via cytokine production; (ii) functioning as regulatory T (T

185 vated, as measured by CD154 upregulation and cytokine production in a CD1c-specific manner.

186 -122, -133a, -142, -146a, and -208a) induced cytokine production in a dose-dependent manner.

187 and CD8(+) cells and inhibited inflammatory cytokine production in a manner that was abrogated by an

188 clearance, and attenuating pro-inflammatory cytokine production in a murine model of lethal sepsis.

189 ectively block cell proliferation in cancer, cytokine production in acute inflammation, and so forth.

190 kappaB activation and caused proinflammatory cytokine production in alveolar macrophages.

191 at Sema4C is critical for optimal regulatory cytokine production in CD138(+) B cells.

192 related to worse asthma control and greater cytokine production in children.

193 was also demonstrated by the attenuation of cytokine production in colonic epithelial cells in vitro

194 BPA into the culture medium and induced more cytokine production in cultured PBMCs than did polynephr

195 module is essential to mediate IL-33-induced cytokine production in dendritic cells.

196 apoptosis and its effect on proinflammatory cytokine production in early alcoholic liver disease has

197 In addition, more Th1 and less Th2 cytokine production in exposed splenocyte, were evident

198 and ozone also interacted to promote type 2 cytokine production in gammadelta T cells and ILC2 in th

199 ecretion, inflammatory cell recruitment, and cytokine production in H2 R-deficient or famotidine-trea

200 timulated TLR4 activation and TLR4-dependent cytokine production in human and mouse cells.

201 d migration, reduced apoptosis, and promoted cytokine production in human ILC2s in vitro.

202 both pro-inflammatory and anti-inflammatory cytokine production in macrophages.

203 TLR4 completely abolished ML exosome-induced cytokine production in macrophages.

204 merged as a key regulator of proinflammatory cytokine production in microglia, functioning as an impo

205 RNA stability, and translation efficiency on cytokine production in murine effector and memory CD8(+)

206 they were seen to stimulate proinflammatory cytokine production in primary human and murine cells in

207 P-evoked intracellular [Ca(2+)]i signals and cytokine production in response to ATP concentrations th

208 Proliferation and cytokine production in response to both AChR and control

209 alent human IFPs increased proliferation and cytokine production in response to CD200(+) leukemia cel

210 ulating effect by enhancing the inflammatory cytokine production in response to inhaled HDM in mice.

211 mast cell responses, undergo chemotaxis and cytokine production in response to PGD2, but it is unkno

212 d proliferation of CD8(+) and CD4(+) TIL and cytokine production in response to stimulation with poly

213 hat DOCK8 regulates NK cell cytotoxicity and cytokine production in response to target cell engagemen

214 The innate immunoregulator STING stimulates cytokine production in response to the presence of cytos

215 been shown to be required for CD8(+) T cell cytokine production in response to viral infection.

216 ical for regulating MUC1/Muc1 expression and cytokine production in the inflammatory microenvironment

217 edema, increased leukocyte infiltration and cytokine production in the lung tissue.

218 eased microglial activation and inflammatory cytokine production in the retina in vivo and a reductio

219 wild-type S. aureus suppressed inflammatory cytokine production in the skin of female, but not male,

220 We speculate that DMDD inhibits cytokine production in the tumor cells in mice, which le

221 in vitro treatment with IL-33 induced type 2 cytokine production in uterine ILC2s, suggesting that th

222 s attenuated NF-kappaB signaling and reduced cytokine production in vivo.

223 a potent negative regulator of NF-kappaB and cytokine production, in TLR4-stimulated monocytes while

224 heral tumors elicit central pro-inflammatory cytokine production, in turn leading to depression and c

225 MSCs suppressed cytokine production, increased M2 macrophage marker expr

226 Yet, upon TCR/CD3 stimulation, while cytokine production increases within a wide range of sti

227 promotes the activation of MKK4 and JNK and cytokine production independently of RIPK1 kinase activi

228 reatment of DOCK8-deficient NK cells rescued cytokine production, indicating a defect proximal to rec

229 We investigated the cytokine production induced by beta2GPI in activated T c

230 nomics approaches reveal the architecture of cytokine production induced by Borrelia infection of hum

231 In mice, the compound inhibited cytokine production induced by injection of several diff

232 ular pattern (PAMP)-induced pro-inflammatory cytokine production, inhibit NF-kappaB p65 activation, a

233 Cytokine production is a necessary event in the immune r

234 Cytokine production is determined by transcriptional and

235 In conclusion, the magnitude of LPS-elicited cytokine production is not indicative of antimicrobial i

236 this article, we show that the IL-33-induced cytokine production is only partly dependent on p65.

237 ocyte activation could contribute to massive cytokine production, known to mediate tissue damage obse

238 ocyte activation could contribute to massive cytokine production, known to mediate tissue damage.

239 on ILC2s impaired early Th2 polarization and cytokine production, leading to delayed worm expulsion d

240 une-response-associated processes, including cytokine production, lymphocyte activation and chemotaxi

241 H2 cytokines or with an inhibitor of pro-TH2 cytokine production might be able to suppress establishe

242 alveolar injury, lung inflammation, induced cytokine production, neutrophil accumulation, and vascul

243 argets affected in vitro monocyte and T-cell cytokine production, neutrophil reactive oxygen species

244 D-1 intrinsically controls proliferation and cytokine production of both mouse and human ILC-2s.

245 stically, this was associated with increased cytokine production of CD8+ CAR T cells and increased ac

246 rations in activation markers, and inhibited cytokine production of freshly isolated T cells or T cel

247 +) ILC3s resulted in increased expansion and cytokine production of intestinal ILC3s and protection a

248 tetraenoic acid promoted M2 polarization and cytokine production of macrophages and thereby enhanced

249 endent T cell activation assays, but shifted cytokine production of T cells from a Th1 (IFN-gamma) to

250 o cytokines, low degranulation, and impaired cytokine production on interaction with tumor targets.

251 e S1P, the sphingosine analogs do not induce cytokine production on their own.

252 es not rely on tetramers, antigen-stimulated cytokine production, or proliferation but rather on anti

253 In addition to impaired T-cell cytokine production, ORAI1 mutations were associated wit

254 vated protein kinase-related proinflammatory cytokine production (P < .0007).

255 We measured cytokine production, proliferation, and differentiation

256 ILC3 cytokine production, proliferation, and differentiation

257 ormed in the absence of APC on CD4(+) T cell cytokine production, proliferation, and expression of ac

258 ved metabolic defects coincided with reduced cytokine production, proliferation, and migration, as we

259 pened PMA-induced ear edema, proinflammatory cytokine production, reactive oxygen and nitrogen specie

260 blood was collected from children to measure cytokine production relevant to asthma (secondary outcom

261 inflammatory effector cell types involved in cytokine production, removal of self-antigens, and respo

262 However, neutrophil cytokine production required STIM2, but not STIM1, at le

263 Although Ag-specific cytokine production requires a glycolytic switch for opt

264 A significantly weakened Ag-specific recall cytokine production response was also found for I-A(12%)

265 shes normal homeostasis, and proinflammatory cytokine production returns to baseline.

266 uating the kinetics of viral replication and cytokine production revealed differences between the mou

267 7 cells were more polyfunctional in terms of cytokine production than either Th1 or bona fide Th17 ce

268 an be reversed by inhibition of inflammatory cytokine production that can be used to promote vaccine

269 luding the regulation of cell proliferation, cytokine production, the innate immune response, and apo

270 opulation with increased TCR sensitivity and cytokine production, they do not reexpand upon reexposur

271 novel mechanism by which it regulates type-2 cytokine production through its modification of the Th2

272 we report that ExoY inhibits proinflammatory cytokine production through suppressing the activation o

273 hts into the posttranslational regulation of cytokine production through the posttranscriptional cont

274 omodulator that provides early type 1-skewed cytokine production to control the parasite load and alt

275 egulator of antiviral immunity that controls cytokine production to restrict viral pathogenesis.

276 gnificantly reduced blood bacterial density, cytokine production (tumor necrosis factor alpha, interl

277 y exhibit dampened proliferation and reduced cytokine production upon activation.

278 subjects, were not anergic and had high TH2 cytokine production upon peanut-specific restimulation.

279 Cytokine production was assessed after stimulation.

280 etabolic studies indicated that the enhanced cytokine production was associated with marked metabolic

281 Higher Vdelta2 pro-inflammatory cytokine production was associated with protection from

282 gous, NTHi-specific lung CD4(+) T cells, and cytokine production was inhibited by a HLA-DR blocking A

283 s and attenuate LPS-induced pro-inflammatory cytokine production was inhibited by buthionine sulfoxim

284 In contrast, R848- and CpG-induced cytokine production was less influenced by the IFNAR-STA

285 Cytokine production was measured by using ELISA, and rea

286 Importantly, we found that licensing of cytokine production was mediated by paracrine TNF-alpha-

287 We confirmed that Ag-specific cytokine production was positively correlated with CD154

288 ed that Acanthamoeba-induced proinflammatory cytokine production was through MyD88-dependent, TRIF-in

289 Activated T cells and their cytokine production were accordingly decreased by Keap1

290 Similar increases in cytokine production were also seen in cultured, IFN-gamm

291 genes that enhanced Th2 polarization and Th2 cytokine production were also upregulated in asthma.

292 strains, and yet, neutrophil recruitment and cytokine production were lower than those with P. aerugi

293 igen-driven T-cell proliferation and TH1/TH2 cytokine production were suppressed (P < 0.05).

294 HDV-specific T-cell proliferation and cytokine production were weak and could only partly be r

295 zed Th subsets to some level, how it impacts cytokine production when effector T cells are restimulat

296 fective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro

297 t strain induces heightened pro-inflammatory cytokine production, which is diminished in the absence

298 d CD8(+) proliferation, but not the effector cytokine production, which modestly increased with TIM-3

299 interferon-regulated genes and dysregulated cytokine production; which are indicative of signalling

300 pansion, and greatly reduced proinflammatory cytokine production, without effecting degranulation and