ライフサイエンスコーパス: cytokine

1 basis for a simplified yet functional IL-12 cytokine.

2 g upd3, highlighting a crucial role for this cytokine.

3 d hyperproduction of inflammasome-associated cytokines.

4 omplex that amplified downstream signals and cytokines.

5 gnificantly increased levels of inflammatory cytokines.

6 f circulating or intra-alveolar inflammatory cytokines.

7 nhibits expression/secretion of inflammatory cytokines.

8 te in vivo in the absence of exogenous human cytokines.

9 behind its downregulation by proinflammatory cytokines.

10 lial cells under the control of inflammatory cytokines.

11 ated blood and BM plasma levels of T helper1 cytokines.

12 arcodes uniquely labeling each of the tested cytokines.

13 igher levels of circulating pro-inflammatory cytokines.

14 n the airways and expression of pro-fibrotic cytokines.

15 XCL9, CXCL10, and downstream proinflammatory cytokines.

16 n associated with a large local secretion of cytokines.

17 icates the skin as the source of circulating cytokines.

18 rve (GSN), and elevation of pro-inflammatory cytokines.

19 y-seven miRNAs were detected as modulated by cytokines.

20 Cytokine activation of endothelial cells (EC) upregulate

21 Here, we show that the cytokine activin-A instructs the generation of CD4(+) T

22 3 (30 ng/mL), a member of the IL-1 family of cytokines, administered in combination with SP (1 microM

23 Cytokine administration resulted in significant reversal

24 (+)-lineage fate is thought to be induced by cytokines after TCR signaling has ceased, although this

25 was induced by prolonged exposure to IL6, a cytokine also generated by the tumor-stroma.

26 While the cytokine and cellular pathways triggering arthritis are

27 s IRAK-3, is an inhibitor of proinflammatory cytokine and chemokine expression in intrarenal macropha

28 Serum cytokine and chemokine levels were measured at baseline

29 e directly investigated the role of prenatal cytokine and chemokine profiles on neurodevelopmental ou

30 iRhom2 is a primary regulator of stimulated cytokine and growth factor signalling.

31 nterleukin-1beta (IL-1beta), an inflammatory cytokine and IL-1 receptor ligand, has diverse activitie

32 Cytokine and immune checkpoint blockade immunotherapy fo

33 n human ILC2 proliferation and intracellular cytokine and transcription factor expression were assess

34 Type 2 innate lymphoid cells (ILC2) share cytokine and transcription factor expression with CD4(+)

35 a high-resolution structure of this critical cytokine and we reveal its functional interaction interf

36 ome hyperactivated, produce pro-inflammatory cytokines and act as more potent antigen presenting cell

37 ssion and down-regulation of proinflammatory cytokines and adhesion molecules.

38 ntrations of inflammatory signals, including cytokines and C-reactive protein, have been described in

39 in modulating LPS-induced expression of many cytokines and chemokines and in modulating Rab7B and P2R

40 ulation in AMPhi augmented the expression of cytokines and chemokines in response to sequential chall

41 increased the mRNA and protein expression of cytokines and chemokines in WT and TLR4-KO mice.

42 lasma or cerebrospinal fluid (CSF) levels of cytokines and chemokines predicted C-IRIS and are potent

43 a and CSF collected pre-ART were assayed for cytokines and chemokines using a 17-plex Luminex kit or

44 Levels of cytokines and chemokines were compared between groups us

45 ced significant increases in proinflammatory cytokines and chemokines.

46 S had exacerbated levels of pro-inflammatory cytokines and exhibited significantly worsened behaviora

47 Circulating cytokines and growth factors are regulators of inflammat

48 f JAK2, a key mediator downstream of various cytokines and growth factors.

49 articles that do not induce pro-inflammatory cytokines and high levels of interferons can be used as

50 Nlrp3 leads to synthesis of proinflammatory cytokines and influences epithelial integrity of cholang

51 tibodies, reduced levels of pro-inflammatory cytokines and innate immune cells.

52 aluated associations between proinflammatory cytokines and lung cancer risk.

53 similar, however, the levels of inflammatory cytokines and MDSC were more pronounced post-cART.

54 in homeostasis by producing antiinflammatory cytokines and neurotrophic factors, support myelin produ

55 ole blood cells to release anti-inflammatory cytokines and neurotrophins.

56 vealed differential response to inflammatory cytokines and other RNABPs.

57 uction of cytotoxic or apoptosis-sensitizing cytokines and promotion of antitumor T cell responses.

58 but preferentially express immunosuppressive cytokines and show an altered metabolism.

59 r pairings that are not formed by endogenous cytokines and that are not found in nature, and which ac

60 nchial epithelial TJs by TH2 cells and their cytokines and their involvement in epigenetic regulation

61 yte migration plus genes for proinflammatory cytokines and various toll-like receptors were overexpre

62 innate lymphoid cells (ILC2s) produce type 2 cytokines, and although advances have been made in under

63 used to assess the production of IgE, type 2 cytokines, and Ccl24.

64 induced robust expression of proinflammatory cytokines, and end products of lipid oxidation had a syn

65 s, elevated serum pro- and anti-inflammatory cytokines, and evidence of innate cell activation that i

66 ar to ECM proteins, matrix-bound chemokines, cytokines, and growth factors (GFs) influence functional

67 ), become activated, produce proinflammatory cytokines, and recruit monocytes and dendritic cells to

68 lls with local production of proinflammatory cytokines, and subsequent epithelial disorders and mitoc

69 alysis demonstrated that pathways related to cytokine- and chemokine-related pathways but also osteoc

70 ration and the secretion of pro-inflammatory cytokines are involved in the propagation of DED-associa

71 pe, with increased secretion of inflammatory cytokines as well as chemokines.

72 ed as a checkpoint regulator of inflammatory cytokines, as well as an inflammasome activator.

73 ndritic cells that produce more inflammatory cytokines both at baseline and following endotoxin expos

74 changes by semiquantitative evaluation, and cytokines by Luminex assay.

75 can be targeted to inhibit the secretion of cytokines by modulating either CXCR4 or CXCR4-mediated s

76 filtrates and suppression of proinflammatory cytokines), cardiac fibrosis, apoptosis, lower CAR (Coxs

77 ligands have an increased ability to produce cytokines, chemokines, and lipid mediators in response t

78 nd in vivo to quantify the spatial extent of cytokine communications in dense tissues.

79 tion but promoted inductions of inflammatory cytokines, compared to wild type hearts.

80 of several signaling pathways, including the cytokine-cytokine receptor interaction pathway, which ca

81 (LoPCB) approach, for TB diagnosis based on cytokine detection.

82 ted epigenetic programs are preserved during cytokine-driven subset interconversion of human memory C

83 ling by all six of these 'lineage-specifying cytokines' during positive selection eliminated Runx3d e

84 m the lungs A. alternata-challenged mice are cytokine-enriched compared to those from IL5tg mice, inc

85 adelta T cell receptor [gammadelta-TCR]) and cytokines examined (interleukin 2 [IL-2], IL-4, IL-10, I

86 in a high degree of cell-to-cell variance in cytokine exposure.

87 Siglec-E16 enhanced proinflammatory cytokine expression and bacterial killing in macrophages

88 Here we show that SOCS3-dependent cytokine expression regulates bone corticalization.

89 Additionally, cytokine expression was examined in the serum (protein),

90 out the TL1A-response pathways that regulate cytokine expression.

91 etabolic pathways, but also the increases in cytokine expression.

92 IL-19, a member of the IL-10 cytokine family that signals through the IL-20 receptor

93 ed maturation medium supplemented with three cytokines (FGF2, LIF, and IGF1) in combination, so-calle

94 kin (IL)-13 is a pleiotropic T helper type 2 cytokine frequently associated with asthma and atopic de

95 on of the thymic microenvironment via type 2 cytokines from innate T cells.

96 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were

97 t in part as a result of redox regulation of cytokine gene expression.

98 naive cells, the regulatory elements of the cytokine genes in the memory T cells are marked by activ

99 evated T cell expression of the inflammatory cytokine GM-CSF, concomitant with pancreatic infiltratio

100 marrow (BM) to the blood circulation by the cytokine granulocyte colony-stimulating factor (G-CSF) t

101 crease in mRNAs encoding various chemokines, cytokines, growth factors, and angiogenesis mediators, w

102 ased gene expression of the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-1beta and RANTES and

103 The cytokine IL-10 has potent antifibrotic effects in models

104 release of the regulatory/anti-inflammatory cytokine IL-10.

105 d identify cellular sources of the signature cytokine IL-13.

106 ticle, we show that LSK(-) cells produce the cytokine IL-17 in response to Plasmodium infection.

107 d have high brain levels of the inflammatory cytokine IL-1beta.

108 a plasmatic increase of the pro-inflammatory cytokine IL-1beta.

109 zed for the expression of the TH2-polarizing cytokine IL-4 and the T-cell activation markers CD69 and

110 addition, the levels of the immunomodulatory cytokines IL-1alpha and IL-10 were significantly decreas

111 1-dependent secretion of the proinflammatory cytokines IL-1beta and IL-18.

112 tinct from those activated by the endogenous cytokines IL-2, IL-4, and IFN.

113 limit the production of the proinflammatory cytokines IL-6 and IL-12p40 while enhancing the release

114 s including release of IL-33, which promotes cytokine (IL-5, IL-13) production by type 2 innate lymph

115 s (IL-4, IL-5 & IL-13) and anti-inflammatory cytokines (IL-10) in the bronchoalveolar fluid, and IL-2

116 nd upregulated expression of proinflammatory cytokines (IL-1beta and TNFalpha).

117 MNs-CIT regulated Th2 cytokines (IL-4, IL-5 & IL-13) and anti-inflammatory cyt

118 vivo neutralization of these proinflammatory cytokines impaired bacterial clearance and eliminated ho

119 ) T cells are being elucidated, with several cytokines implicated.

120 GM-CSF has been portrayed as a critical cytokine in the pathogenesis of experimental autoimmune

121 strated by reduced secretion of inflammatory cytokines in affected skin tissue from NC/Nga mice.

122 ure IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines in CD4(+) and CD8(+) T cells.

123 ssays are essential for characterizing human cytokines in healthy subjects.

124 To study IL-17-related cytokines in nasal/bronchial biopsies from controls and

125 to display increased levels of inflammatory cytokines in peripheral and central tissues.

126 Expression analyses of cytokines in peritoneal tissue and fluid and in vitro as

127 ity of leukocytes to release proinflammatory cytokines in response to ex vivo stimulation.

128 l pulp expresses a range of pro-inflammatory cytokines in response to the infectious challenge.

129 ronchoalveolar fluid, and IL-2 and IFN-gamma cytokines in restimulated splenocyte cultures.

130 re believed to function as anti-inflammatory cytokines in T1D.

131 In addition, H5N1 virus induced cytokines in the heart, pancreas, spleen, liver, and jej

132 a provide evidence implicating CD4(+) T-cell cytokines in the pathogenesis of RCDII.

133 is a pleiotropic signaling mediator of many cytokines, including interleukin-6 (IL-6) and IL-10.

134 ciated with increased levels of inflammatory cytokines, including tumor necrosis factor (TNF).

135 icating their innate nature and their gammac cytokine independence.

136 evations in cutaneous and serum inflammatory cytokines induced by epidermal dysfunction.

137 beta-cells, broadening our understanding of cytokine-induced beta-cell apoptosis in early T1D.

138 e functions as a transcriptional effector of cytokine-induced IKKbeta signaling, suggesting a mechani

139 atment of AAT deficiency, inhibits IBMIR and cytokine-induced inflammation in islets.

140 plex) is not essential for the inhibition of cytokine-induced JAK/STAT signalling activation in DF-1.

141 strong interferon and mild pro-inflammatory cytokine induction may qualify as vaccine adjuvants.

142 uld be differentially regulated by epidermal cytokine induction of specific IRF-controlled pathways.

143 -12 and thereby blocks the activity of these cytokines, inhibiting interleukin-23-dependent productio

144 ar defects, as well as low production of the cytokine interferon-gamma (IFN-gamma).

145 Increased level of proinflammatory cytokine interleukin (IL)-12 correlates with the severit

146 ile monocytes expressed the pro-inflammatory cytokine interleukin-1beta (IL-1beta).

147 lso inhibits release of the pro-inflammatory cytokine interleukin-1beta from activated microglia, con

148 show enhanced production of proinflammatory cytokines (interleukin-3, interleukin-6, interleukin-13,

149 tor (AR) is not detected (AR-), whereas this cytokine is uniformly absent in the AR-positive (AR+) me

150 In vivo loss of STIM2 results in lower cytokine levels and protection from mortality in a mouse

151 ed similar elevations in epidermal and serum cytokine levels in normal and athymic mice, suggesting t

152 dies have examined differences in individual cytokine levels in patients with chronic liver disease,

153 tabolomics signatures, cell populations, and cytokine levels, and identifies immune and metabolic cor

154 Based on the brain cytokine levels, MAV-1-infected Unc93b1(-/-) mice had a

155 eased the anti-inflammatory (IL-10 and IL-4) cytokine levels.

156 cyte development and differentiation rely on cytokines, many of which signal through the JAK/STAT sig

157 e suggests a crucial role of inflammation in cytokine-mediated beta-cell dysfunction and death in typ

158 ntially involved in the increased T-helper 1 cytokine-mediated inflammatory damage in heart.

159 f IL-10R signaling in preventing T-cell- and cytokine-mediated pathology during potentially lethal ma

160 s known about mechanisms that restrain IL-17 cytokine-mediated signaling, particularly IL-17C.

161 lance between IL-12/IL-23 subunits causing a cytokine milieu rich in IL-23 to favour Th2 polarization

162 advances have been made in understanding the cytokine milieu that promotes ILC2 responses, how ILC2 r

163 The fibrotic process is initiated by cytokines, neuroendocrine effectors, and mechanical stra

164 +) T cells is to produce CXCL8, a prototypic cytokine of innate immune cells.

165 IL-37, a newly found anti-inflammatory cytokine of the IL-1 family, has both extracellular and

166 IL-33 is an instructive cytokine of type 2 inflammation whose expression is asso

167 ere we develop AcTakines (Activity-on-Target cytokines), optimized (mutated) immunocytokines that are

168 rat, mouse, and human beta-cells exposed to cytokines or thapsigargin-induced ER stress.

169 nal trials of medications aimed at targeting cytokine overactivity that act directly on brain functio

170 ntestinal tract that are driven by perturbed cytokine pathways.

171 Cytokines play a critical role in directing the discrete

172 Cytokine priming was required to elicit the unanticipate

173 After cytokine priming, Siglec-8 mAb or glycan ligand binding

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 ILC3 cytokine production, proliferation, and differentiation

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

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

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

195 erturb this response, resulting in decreased cytokine production.

196 hallenged wild-type mice maintain a distinct cytokine profile, and, unlike eosinophils isolated from

197 The comparison of the inflammatory response, cytokine profiles and Th-1, Th-2 and Th-17 cells numbers

198 We examined serum cytokine profiles of 411 patients with HCC (n = 102: 32%

199 th or without HCC, have distinctly different cytokine profiles, suggesting potential differences in d

200 according to their transcription factor and cytokine profiles.

201 tent viral blips, were associated with these cytokine profiles.

202 ith chronic liver disease, but comprehensive cytokine profiling data across different clinical charac

203 terized by genomic alterations that activate cytokine receptor and kinase signaling.

204 okines (synthekines) that drive formation of cytokine receptor dimer pairings that are not formed by

205 lisib resulted in near eradication of ALL in cytokine receptor-like factor 2 (CRLF2)/JAK-mutant model

206 eukemia virus (MPL), abnormally activate the cytokine receptor/JAK2 pathway and their downstream effe

207 anus kinase (JAK) inhibitors have shown that cytokine receptors that signal through the JAK/STAT sign

208 ogen-associated molecular pattern receptors, cytokine receptors, adipokine receptors, and hormones.

209 Our findings provide insight into cytokine recognition by the IL-10R family and highlight

210 These cytokines regulate central nervous system neurons to ind

211 ous polypharmacological studies on chemokine/cytokine release from human macrophages, the prostanoid

212 ver, Cu- and Zn-AMSs enhanced maturation and cytokine release of bone marrow dendritic cells in vitro

213 Grade 3-4 cytokine release syndrome occurred in 46% of patients fo

214 Twenty patients (83%) developed cytokine release syndrome, and eight (33%) developed neu

215 patterns leading to caspase-1 activation and cytokine release, which mediate protective innate immune

216 ors, which prevents caspase-1 activation and cytokine release.

217 ight were tested for their ability to induce cytokine response in macrophages and cardiomyocytes.

218 of blood monocytes with less proinflammatory cytokine response to bacterial stimulation and less huma

219 numbers and IgE antibody levels, but type 2 cytokine responses and eosinophilic inflammation in the

220 lts suggest that those who possess activated cytokine responses beyond the current treatment criteria

221 in urban homes stimulate the development of cytokine responses in early life, and that cytokine resp

222 The decreased cytokine responses in R753Q TLR2-expressing macrophages

223 s in parallel with analysis of local mucosal cytokine responses induced by nasal allergen exposure an

224 te having significantly reduced inflammatory cytokine responses to LPS and bacterial infection, POP2

225 f cytokine responses in early life, and that cytokine responses to specific microbial and viral stimu

226 Cytokine responses were measured in blood cell samples o

227 ant inverse associations with several type 2 cytokine responses.

228 oduction of proinflammatory and TH17-skewing cytokines, resulting in a TH17 immune response with IL-2

229 mut) induced lower levels of proinflammatory cytokines, resulting in viral attenuation in vivo This m

230 -7 breast cancer cells with pro-inflammatory cytokines results in ERalpha-dependent activation of gen

231 s, apoptotic markers, and human inflammatory cytokines returned to pretreatment levels within 9 days

232 Analysis of the immune response via cytokines revealed that dexamethasone was important for

233 Therefore, we studied B cell cytokine secretion and/or Ab production across obesity m

234 ent the importance of PKR, TRIF, and TBK1 in cytokine secretion during L. pneumophila infection of ma

235 AMA0825 did not affect pro-inflammatory cytokine secretion from other ROCK-positive cell types,

236 8.0 trauma, p < 0.05) and reduced leukocyte cytokine secretion in response to lipopolysaccharide sti

237 (mtDNA) integrity, morphology, phenotype and cytokine secretion into storage buffer.

238 li modulating amino acid catabolism, as were cytokine secretion levels and regulatory T cell numbers.

239 Furthermore, reduced cytokine secretion observed at high Ag density for both

240 osomal proteins and inducing proinflammatory cytokine secretion through protease-activated receptor 2

241 in upregulation of antiapoptotic molecules, cytokine secretion, and enhanced effector function.

242 155 (miR-155) and its target, suppressor of cytokine signaling 1 (SOCS-1).

243 1 is a critical effector of pro-inflammatory cytokine signaling and plays important roles in immune f

244 ddition of IL-12 to cultures, revealing that cytokine signaling could restore the acquisition of effe

245 How structural dynamics affects cytokine signaling is under debate.

246 controlling TLR4 signaling and inflammatory cytokine signaling through a negative feedback regulatio

247 contribute to treatment tolerance through a cytokine-signaling network that involves macrophage-deri

248 y mediators implicated in the TSS-associated cytokine storm.

249 ift hyperinflammatory response typified by a cytokine storm.

250 othelial barrier disruption and uncontrolled cytokine storm.

251 TCR and respond instead to locally produced cytokines such as IL-33.

252 th factors such as VEGF and pro-inflammatory cytokines such as TNF-alpha.

253 s and chemokines induced by pro-inflammatory cytokines such as TNFalpha and IFNgamma, but the regulat

254 ming the pathogenetic function of additional cytokines (such as the interferons).

255 d by key transcription factors and output of cytokines, such as IL-4, IFN-gamma, IL-17, and IL-10.

256 well as increased levels of proinflammatory cytokines, such as TNF-alpha and IL-17.

257 pe-specific amplification of proinflammatory cytokines, such as TNF-alpha, IL-1beta, IL-6, and IL-23.

258 ivo in the absence of exogenous pro-survival cytokine support.

259 We have engineered synthethic cytokines (synthekines) that drive formation of cytokine

260 n, immunoglobulin production, TH2-associated cytokine synthesis, and pulmonary dendritic cell activit

261 Levels of anti-inflammatory cytokine TGF-beta remained practically unaffected in ImI

262 lic activity and release of pro-inflammatory cytokines than CFC tissue, but surprisingly, more active

263 S. agalactiae produced less proinflammatory cytokines than those infected with wild-type 874391.

264 We identified IL-18 as a cytokine that cooperates with an ILC3 survival factor, I

265 TNF-alpha is a pluripotent cytokine that has been independently involved in the pat

266 Interleukin-15 is a pleiotropic cytokine that is critical for the development and surviv

267 IL-37 is a novel pro-angiogenic cytokine that potently promotes endothelial cell activat

268 ne motility factor (AMF) is a tumor-secreted cytokine that stimulates tumor cell motility in vitro an

269 Human cytomegalovirus encodes 2 viral cytokines that are orthologs of human cellular interleuk

270 tudies, central and blood borne inflammatory cytokines that can be elevated in RA evoke pathogenic in

271 We sought to identify cytokines that can promote proliferation and induce or m

272 immune-based therapies; in addition to early cytokine therapy, newer checkpoint inhibition therapies

273 r tissue damage through expression of type 2 cytokines thereby participating in the pathogenesis of i

274 recovery after SCI by dampening inflammatory cytokines, thus pointing towards a new direction of immu

275 ody specific for the epithelial-cell-derived cytokine thymic stromal lymphopoietin (TSLP), in patient

276 We verified the oncogenic role of the cytokine tissue inhibitor of matrix metalloproteinases 1

277 sible for the liberation of the inflammatory cytokine TNFalpha and ligands of the epidermal growth fa

278 that granulocytes are the main source of the cytokine TNFalpha, whereas its receptor TNFR1 is selecti

279 Plasma levels of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha) are incr

280 associated with high levels of inflammatory cytokines: tumor necrosis factor, interleukin (IL)-6, an

281 eficient mice displayed high levels of serum cytokines typifying profound autoinflammation.

282 tivated monocytes to produce proinflammatory cytokines, up-regulated their C5aR and FcRIII expression

283 ng in epithelial expression of the IL-6-like cytokine Upd3, leading to activation of JAK/STAT signali

284 ongly reduced the production of inflammatory cytokines upon stimulation with aminobisphosphonate-trea

285 ggest that NRTIs up-regulate proinflammatory cytokines via a Wnt5a signaling-dependent mechanism.

286 n FEV1 , Pc20, airway inflammation and serum cytokines was investigated.

287 Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfe

288 ed proteomic profiling of over 100 different cytokines, we found that Lipocalin-2 (LCN2) was the most

289 tive factor Kruppel-like factor 2 (KLF2) and cytokines were also studied using similar approaches.

290 lso collected and levels of IL-33 and type 2 cytokines were measured.

291 Plasma levels of 17 cytokines were screened in the same set of subjects.

292 Thus, the novel IL233 hybrid cytokine, which utilizes the cooperation of IL-2 and IL-

293 teroreceptor (HR) serves both IL-4 and IL-13 cytokines, which are believed to function as anti-inflam

294 cells curtails production of proinflammatory cytokines, which are otherwise detrimental for survival

295 her baseline serum concentrations of IL22, a cytokine whose expression is induced by IL23, were assoc

296 ceptor type I (IL-20Ralpha:IL-20Rbeta), is a cytokine whose function is not completely known.

297 IL6 is a pleiotropic cytokine with both pro- and anti-inflammatory properties

298 epigenetic hotspot regulated by IL-13, a TH2 cytokine with increased levels in patients with EoE that

299 om Cmah(-/-) mice secreted more inflammatory cytokines with LPS stimulation and showed more phagocyti

300 nts with elevated pro- and anti-inflammatory cytokines would have higher mortality rates and that the