ライフサイエンスコーパス: IL-10

1 IL-10 deficiency in mice restores protective immunity to

2 IL-10 green fluorescent protein reporter mice revealed t

3 IL-10 is a pleiotropic cytokine expressed during malaria

4 IL-10 is a potent anti-inflammatory mediator that plays

5 IL-10 is an immunomodulatory cytokine with a critical ro

6 IL-10 is an immunoregulatory cytokine that has broad eff

7 IL-10 is an immunoregulatory cytokine, which in other in

8 IL-10 is essential to maintain intestinal homeostasis.

9 IL-10 is responsible for STAT3 activation during the fir

10 IL-10 limits the magnitude of inflammatory gene expressi

11 IL-10 might play a key role in acquisition of tolerance

12 IL-10 receptor alpha is highly enriched in mature adipoc

13 IL-10 serum concentration was higher in SaB patient mort

14 IL-10 was predominantly produced by the CD1d(hi) CD5(+)

15 IL-10-expressing cells were detected among both CD4(+) a

16 IL-10-producing B cells represent a major subset of regu

17 Interleukin 10 (IL-10) is an anti-inflammatory cytokine that plays a cri

18 all peptidoglycan stimulates interleukin 10 (IL-10) production in Staphylococcus aureus bacteremia (S

19 ukin 1beta, CCL5/RANTES, and interleukin 10 (IL-10) were elevated in RSV+ bronchiolitis (all P < .05)

20 tor-alpha, interferon-gamma, interleukin 10 (IL-10), and CXCL9.

21 e anti-inflammatory cytokine interleukin 10 (IL-10), and decreasing that of the pro-inflammatory cyto

22 nterleukin 2, interleukin 6, interleukin 10 (IL-10), and soluble CD14 compared with HEU infants.

23 atment of donor corneas with interleukin-10 (IL-10) and transforming growth factor-beta1 (TGFbeta1) a

24 Interleukin-1b (IL-1b) and interleukin-10 (IL-10) biomarkers are one of many antigens that are secr

25 a interferon (IFN-gamma) and interleukin-10 (IL-10) responses to 6 HCMV peptide pools (pp65, pp71, IE

26 Interleukin-10 (IL-10)-producing B cells (B10 cells) play a critical rol

27 e anti-inflammatory cytokine interleukin-10 (IL-10).

28 e anti-inflammatory cytokine interleukin-10 (IL-10).

29 oxP3(+) Treg, CD19(+)B220(+)CD5(+) IL-10(+), IL-10(+) Tr1, and IL-10(+) TCR gammadelta(+) cells.

30 de dehydrogenase 1A2 but not IL-12 or IL-35; IL-10 and TGF-beta together drove their suppression of T

31 increasing IFN-gamma while decreasing IL-4, IL-10, and Foxp3 expression by CD4(+) T cells-effects th

32 s that allow the improved detection of IL-4, IL-10, IL-13 and IL-17A ex vivo.

33 okines examined (interleukin 2 [IL-2], IL-4, IL-10, IL-17A, and gamma interferon [IFN-gamma]) and ren

34 timulate cytokine TNF-alpha, IL-1beta, IL-6, IL-10, and IL-12 production in human monocytes.

35 the genes for interleukin (IL)-1beta, IL-6, IL-10, monocyte chemoattractant protein-1, tumor necrosi

36 l of inflammatory responses (IL-1beta, IL-6, IL-10, TNF).

37 8, CD206, FOXP3), cytokines (IL-1beta, IL-6, IL-10, TNF-alpha) and oxidative stress (superoxide dismu

38 nt sera with elevated (n = 8) or low (n = 8) IL-10 using a magnetic bacterial capture assay.

39 of interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, IL-12, interferon gamma, tumor necrosis factor al

40 c macrophages, and its activation promotes a IL-10-dependent shift toward an alternatively activated

41 of IFN-gamma and TNF-alpha production, along IL-10 increase, (ii) CD73(+)Foxp3(+)Treg subset expansio

42 Although IL-10 and STAT3 signaling were intact, the antifibrotic

43 A larger proportion of donors produced an IL-10 response to pp71 and US3, but the IFN-gamma respon

44 involvement of macrophages in regulating an IL-10/CREB/WISP-1 signaling axis, with broad implication

45 ene B4, and ELISAs quantified TNF, IL-12 and IL-10 in the gingival tissues.

46 rosis factor (TNF), interleukin (IL)-12, and IL-10 in gingival tissues.

47 ile with increase in CCL22, IL-4, IL-13, and IL-10 in both NLFS and COPDs.

48 tokines, such as IL-4, IFN-gamma, IL-17, and IL-10.

49 the immunomodulatory cytokines IL-1alpha and IL-10 were significantly decreased, and the levels of IL

50 ing patients have more Treg cells, IL-33 and IL-10 in their peripheral blood.

51 Intravitreal injection of IL-4 and IL-10 ameliorated RPE toxicity that was induced by NaIO3

52 at stabilizes interleukin-2(IL-2), IL-4, and IL-10 messenger RNA (mRNA) transcripts.

53 specific production of IFN-gamma, IL-4, and IL-10.

54 n of PD-1, PD-L1, PD-L2, TGF-beta, IL-5, and IL-10 mRNA was measured by real-time quantitative PCR on

55 ytokines, including interleukin-6 (IL-6) and IL-10.

56 wer levels of TNF-alpha, IL-1beta, IL-6, and IL-10 compared with cells from WT mice, but both R753Q T

57 ge, serum levels of TNF-alpha, KC, IL-6, and IL-10 were significantly increased in lyM-PP2A(fl/fl) mi

58 LR stimulation, CD1(+) cDC produced IL-8 and IL-10 while CD1(-) cDC secreted IFN-alpha, IL-12 and TNF

59 nses at age 3 years, including IFN-alpha and IL-10 responses to certain stimulants and responses to p

60 ivation, as well as IL-1beta, TNF-alpha, and IL-10 secretion in vascular endothelial cells.

61 cing the expression of CD39, granzyme B, and IL-10, resulting in the efficacious suppression of ongoi

62 Neutralization of HLA-G, TGF-beta, and IL-10 partially restored T cell alloproliferation, argui

63 tolerogenic molecules (HLA-G, TGF-beta, and IL-10) were tested on a mixed lymphocyte reaction betwee

64 ults in the induction of HO-1, TGF-beta, and IL-10, as well as the repression of NF-kappaB, EDN-1 and

65 of TSLPR(+) mono, including higher CCL17 and IL-10 production and increased expression of genes with

66 hiolitis (all P < .05), furthermore CCL5 and IL-10 correlated with RSV load (P < .05).

67 hough the frequencies of CD1d(hi) CD5(+) and IL-10-producing (IL-10(+)) CD45(+) cells were decreased.

68 0-expressing human CD4(+)CD25(+) T cells and IL-10(+)FoxP3(+) Tregs in mice.

69 phenotype, upregulated FOXP3 expression and IL-10 secretion, and lost pathogenicity in vivo.

70 et, and were able to coproduce IFN-gamma and IL-10 upon ex vivo stimulation.

71 on is associated with induced IFN-gamma- and IL-10-producing regulatory CD4(+)CD25(+) forkhead box p3

72 cytometry, we found that both T. gondii and IL-10 inhibited virus-induced nuclear translocation, but

73 collagen-induced arthritis by using PGRN and IL-10 genetically modified mouse models.

74 exposed to LPS, and serum cytokines (TNF and IL-10) were measured.

75 (+)B220(+)CD5(+) IL-10(+), IL-10(+) Tr1, and IL-10(+) TCR gammadelta(+) cells.

76 th MSC homing and MSC production of VEGF and IL-10, suggesting microenvironmental changes from pFUS a

77 in MS patients, stimulated antiinflammatory IL-10-expressing human CD4(+)CD25(+) T cells and IL-10(+

78 row, CD68 downward arrow, IL-4 upward arrow, IL-10 upward arrow, and TGF-beta upward arrow) and enhan

79 Also, cytokines such as IL-10 and TGF-beta1 significantly reduce cytokine secret

80 on primarily in Treg specialization, because IL-10 production, expression of other effector molecules

81 By using both IL-10-deficient and wild-type mothers, we showed that bo

82 In vivo, both IL-10 mRNA expression and the number of IL-10(+) CD45(+)

83 lt in antigen-specific tolerance assessed by IL-10 measurement and Treg frequency.

84 fibrotic repair phenotype that is induced by IL-10 overexpression was abrogated in this model.

85 e transfer of IL-10(+/+) NK cells and not by IL-10(-/-) NK cells.

86 sregulated interleukin (IL)-10 production by IL-10(+ve) B cells to autoimmunity, highlighting the imp

87 second cluster can be rapidly suppressed by IL-10 even after transcription is initiated, and this is

88 (IL-13, CCL17, eotaxin-1/CCL11, CCL13, CCL4, IL-10), Th1 (CXCL10, CXCL11) and Th1/Th17/Th22 (IL-12/IL

89 doptive transfer of wild-type CD19(+)CD138(+)IL-10(+) cells dramatically decreased allergic airway in

90 The percentages of CD19(+) IL-10(+) cells, CD19(+) CD1d(hi) CD5(+) cells, and P. gi

91 TAT3-dependent up-regulation of FOXp3, CD39, IL-10, and granzyme B, resulting in enhanced suppressive

92 +)CD25(+)FoxP3(+) Treg, CD19(+)B220(+)CD5(+) IL-10(+), IL-10(+) Tr1, and IL-10(+) TCR gammadelta(+) c

93 Consequently, IL-10 promotes mitophagy that eliminates dysfunctional m

94 tal differences in the signaling controlling IL-10 production in B cells and macrophages, even though

95 Conversely, the immunosuppressive cytokine IL-10 has been shown to dampen Th1 cell responses to M.

96 igh levels of the immunosuppressive cytokine IL-10, but not Foxp3, and can suppress inflammation and

97 t ablation of the anti-inflammatory cytokine IL-10 improves insulin sensitivity, protects against die

98 demonstrated that anti-inflammatory cytokine IL-10 was a critical mediator for PGRN-mediated anti-inf

99 production of the anti-inflammatory cytokine IL-10, and vastly improved mouse survival.

100 of the regulatory/anti-inflammatory cytokine IL-10.

101 The cytokine IL-10 has potent antifibrotic effects in models of adult

102 d mucosal immunoglobulin (IgM) and cytokine (IL-10, IL-4) production, thus providing the possibility

103 omposed of the fibrosis-associated cytokines IL-10 and IL-13 and extracellular matrix genes fibronect

104 -5 & IL-13) and anti-inflammatory cytokines (IL-10) in the bronchoalveolar fluid, and IL-2 and IFN-ga

105 Both cytokines: IL-10 and IL-1b were detected within the range of 1pgmL(

106 nt CD19(+)CD138(+) cells exhibited decreased IL-10 and increased IL-4 expression in vivo and in vitro

107 macrophage-depleted mice presented decreased IL-10-mediated myeloid and T cell regulatory responses s

108 ings demonstrate the role for RAGE-dependent IL-10 suppression as a key modulator of mortality from G

109 Foxo4- and Stat3-dependent IL-10 production by progranulin in regulatory T cells re

110 e to superantigens through a TLR2-dependent, IL-10-mediated mechanism.

111 utocrine feedback loop of macrophage-derived IL-10 and this synergized with inhibition of the JNK pat

112 following mucosal injury, macrophage-derived IL-10 resulted in epithelial cAMP response element-bindi

113 ogated in the absence of bone marrow-derived IL-10.

114 se results demonstrate that monocyte derived IL-10 acts to inhibit potentially protective cell mediat

115 oduced into whole blood ex vivo to determine IL-10 production with variable inocula.

116 Double IL-10(eGFP) Foxp3(mRFP) reporter mice and transgenic mic

117 When analyzed longitudinally, an early IL-10 mRNA expression was observed.

118 esults show that H. hepaticus triggers early IL-10 induction in intestinal macrophages and produces a

119 deoxynucleotide (CpG) to determine effective IL-10 induction in vitro Silk ligatures (size 7-0) were

120 Elevated IL-10 serum concentrations at clinical presentation of S

121 By 1 wk, the elevated IL-10 expression remained, and IL-6 expression was signi

122 racranial injections of plasmid DNA encoding IL-10 (pDNA-IL-10) into the NAc of non-handled rats.

123 lyclonal T-cell stimulation, and an enhanced IL-10 response of cord blood mononuclear cells to dexame

124 n of exogenous IL-4 to Th1 cultures enhanced IL-10 production.

125 as phosphorylation of STAT3 further enhances IL-10 expression in human Bregs.

126 s that of wild-type (WT) mice, and exogenous IL-10 administration to WT mice enhances survival in thi

127 ses and placental development in DC expanded IL-10(-/-) dams.

128 infection, the predominant cells expressing IL-10 in the lung were Ly6C(+) monocytes.

129 mature yet tolerogenic phenotype, expressing IL-10, TGF-beta, IL-27, and aldehyde dehydrogenase 1A2 b

130 gery, with over 85% CD146(+) TSCs expressing IL-10.

131 Finally, IL-10-producing drug-specific T cell clones downregulate

132 T cells are the major source accounting for IL-10-induced TB susceptibility.

133 ry disease; however, the molecular basis for IL-10-mediated inhibition remains elusive.

134 Although TIM-1(+) B cells are enriched for IL-10, TIM-4(+) B cells are enriched for IFN-gamma.

135 f transcription is the primary mechanism for IL-10-mediated suppression in LPS-stimulated macrophages

136 Thus, a key pathway for IL-10-mediated suppression involves rapid inhibition of

137 ists, neither MSKs nor CREB are required for IL-10 production in these cells.

138 hanistic analyses revealed a requirement for IL-10 in LPS-mediated decrease in MC FcepsilonRI surface

139 nt study, we demonstrate divergent roles for IL-10 depending on the site of infection.

140 Furthermore, IL-10 suppresses mammalian target of rapamycin (mTOR) ac

141 At delivery, high IL-10 levels in maternal blood were associated with an i

142 arts, and this effect associated with higher IL-10 concentration and regulatory T cell-to-leukocyte r

143 ies (mAb) of anti-human IL-1b and anti-human IL-10 were electroaddressed onto the gold WEs through fu

144 r the expansion and differentiation of human IL-10-producing Bregs.

145 tion of the anti-inflammatory mediators IDO, IL-10, and PGE2 in a COX-2-dependent manner.

146 s in the first cluster are inhibited only if IL-10 is included early in the course of LPS stimulation

147 TR1 cells with impaired IL-10 receptor signaling lost their regulatory activity

148 the gain-of-function mutation of TTP impairs IL-10-mediated negative feedback control of macrophage f

149 Remarkably, DC expansion in IL-10(-/-) dams provoked pregnancy loss, which could be

150 mice and transgenic mice with impairment in IL-10 receptor signaling were used to test the activity

151 atory phenotype in DCs - with an increase in IL-10 and higher expression of programmed death ligand (

152 the presence of CM-MSC or MSCs, increases in IL-10 concentration were observed in culture medium.

153 d that anti-inflammatory cytokines including IL-10 and IL-11 as well as FOXP3 were upregulated in the

154 In addition, increased IL-10 expression appears to be due to PP2ACalpha-knockou

155 flammatory cytokine production and increased IL-10 production.

156 1 in CD8alpha(+) DCs significantly increases IL-10 expression, reduces macrophage and T-cell contents

157 mentation of IL-27 activates Egr-2 to induce IL-10 producing Tr1 cells.

158 o data, AngII synergized with BAFF to induce IL-10 production by B cells in vitro via AngII type 1A r

159 vely, these studies suggest that LPS-induced IL-10 promotes the down-regulation of MC surface Fcepsil

160 g the clinical outcomes, reduced LPS-induced IL-10 responses at birth were associated with recurrent

161 ll, but was not due to peptidoglycan-induced IL-10 production.

162 conventional dendritic cells (cDC), inducing IL-10, and promoting development of regulatory Tr1 cells

163 n synergy between AngII and BAFF in inducing IL-10 production by B cells, resulting in atheroprotecti

164 n contrast, during localized s.c. infection, IL-10 production plays a detrimental role by facilitatin

165 ncreased the expression of anti-inflammatory IL-10 at 2 d after surgery, with over 85% CD146(+) TSCs

166 suppressing production of anti-inflammatory IL-10 by lung CD11b(+)Ly6G(int)Ly6C(lo)F4/80(+) cells.

167 vealed that the epithelial anti-inflammatory IL-10 receptor alpha subunit (IL-10RA) is also important

168 ecreased the production of anti-inflammatory IL-10, and stimulated the secretion of IL-6.

169 -1beta) and increased the anti-inflammatory (IL-10 and IL-4) cytokine levels.

170 ulatory T cells and IFN-gamma and inhibiting IL-10 production.

171 In the absence of an intact IL-10 signaling, H. hepaticus induces an IL-23-driven in

172 sis by converting resting B and T cells into IL-10-producing and IL-35-producing regulatory B (Breg)

173 ogether, our data show that B cell-intrinsic IL-10 enhances whereas B cell-intrinsic IFN-gamma and T-

174 ell population, where the tolerance state is IL-10 dependent.

175 OATP1a1, and ileum ASBT and decreased liver IL-10, FXR, CAR, VDR, BSEP, MRP2, MRP3, MRP4 was also ob

176 th elevated serum IL-10 vs patients with low IL-10 (35.5 vs 0.5 median CFU/mL; P = .044).

177 exacerbated proinflammatory responses (lower IL-10 and CCL2, higher TNF-alpha, IL-6, and IL-1beta) to

178 umigatus extract-induced inflammation model, IL-10-producing CD4(+) T cells in bronchoalveolar lavage

179 at express the Tr1-cell-associated molecules IL-10, inducible T-Cell costimulator (ICOS), lymphocyte

180 Blocking neither IL-6Ralpha/IL-6 nor IL-10 affected ESAT-6-induced STAT3 activation and IL-6

181 In the absence of IL-10, Helicobacter hepaticus (Hh) induces colitis.

182 wild-type (WT) cultures, and the addition of IL-10 eliminated the difference in IgE production betwee

183 Exogenous administration of IL-10 was sufficient to overcome early pregnancy failure

184 strated B-1a cells produced ample amounts of IL-10 which controlled excessive inflammation and the mi

185 s, Th2 cells produce considerable amounts of IL-10.

186 in Th2 cells by facilitating the binding of IL-10-inducing transcription factors at the Il10 locus.

187 restored IL-10 production and the binding of IL-10-inducing transcription factors including E4BP4, IF

188 elated with prevaccination concentrations of IL-10 (RV5 surface proteins G1 and P1) and IFNgamma (G1)

189 Conditional deletion of IL-10 specifically in CD11c-expressing cells in vivo imp

190 duction, thereby allowing the development of IL-10-dependent tolerance to endotoxin.

191 demonstrate that the regenerative effects of IL-10 in postnatal wounds are dependent on HA synthesis

192 mphocyte proliferation, induces expansion of IL-10-expressing and IL-35-expressing B cells and amelio

193 demonstrated that CTGF-induced expression of IL-10 and TIMP-3 in CD146(+) TSCs are regulated by JNK/s

194 tors known to be important for expression of IL-10, including Jun family members, GATA3, E4BP4, and I

195 ammatory despite the decreased expression of IL-10.

196 The importance of IL-10-induced HA synthesis for regenerative wound healin

197 Our findings demonstrate that induction of IL-10 has a major influence on disease outcome during ac

198 d CREB is indispensable for the induction of IL-10 production, whereas phosphorylation of STAT3 furth

199 In conclusion, we report the induction of IL-10-driven regulatory responses mediated by CD11b(+)F4

200 ack of IL-4Ralpha inhibited the induction of IL-10.

201 n early increase of TNF-alpha and, later, of IL-10.

202 and CpG significantly increased the level of IL-10 production by B cells in vitro, although the frequ

203 Tolerant Treg cell produced high levels of IL-10 and had diverse T cell receptor Vbeta repertoires

204 Lower baseline serum levels of IL-10 and higher tryptase levels were found in active CM

205 High levels of IL-10 and IL-12/23p40 were significantly associated with

206 uction by NK cells and lower serum levels of IL-10 in the MCMV-infected Ebi3(-/-) B6 mice.

207 We found significantly higher levels of IL-10, IL-1beta, IL-4 and IL-2 in both MCI groups (P<0.0

208 XCL9, and iNOS, but increasing the levels of IL-10, LIGHT, CCL1, and Arg-1.

209 er level of bacteremia, is a key mediator of IL-10 anti-inflammatory response that portends poor clin

210 phosphorylate STAT3, a critical mediator of IL-10's anti-inflammatory effects.

211 The neutralization of IL-10 enhanced the activation of a T-cell CD4+ populatio

212 Neutralization of IL-10 in RAGE(-/-) mice results in decreased survival du

213 Neutralization of IL-10 increased IFN-gamma, IL-6 and TNF-alpha production

214 differentiation and increased the number of IL-10(+) CD4(+) T cells, and the conditioned medium from

215 both IL-10 mRNA expression and the number of IL-10(+) CD45(+) cells were significantly increased afte

216 mice with muscle-specific overexpression of IL-10 (M(IL10)) and in wild-type mice during hyperinsuli

217 effect of IL-4 on the natural phenomenon of IL-10 production by a chronically stimulated antigen-spe

218 cells were differentiated in the presence of IL-10 from PBMCs of patients with PA and HC subjects pul

219 tured with B. pseudomallei and production of IL-10 and IFN-gamma detected and the cellular sources id

220 cule interactions and required production of IL-10 and TGF-beta.

221 mice substantially reduced the production of IL-10 by B cells and prevented the AngII-dependent ather

222 IL-17, and IL-22 and decreased production of IL-10 following IL-27 and IL-37 neutralization and paras

223 ithin the cell, as well as the production of IL-10.

224 immunoregulatory cytokine fusion proteins of IL-10/Fc, TGF-beta/Fc, or IL-2/Fc would enhance allogene

225 In a macrophage cell line, regulation of IL-10 by BAR501 was GPBAR1 dependent and was mediated by

226 oving the understanding of the regulation of IL-10 production in these cells.

227 enal macrophages showed increased release of IL-10, whereas tumor necrosis factor and cathepsin L rel

228 although not exclusively, via the release of IL-10.

229 The role of IL-10 in regulating B cell responses during malaria is n

230 tion, thus highlighting a protective role of IL-10(+) regulatory B cells in this setting.

231 Recent data highlight the role of IL-10-producing regulatory B cells and "protective" anti

232 signaling and the TLR-dependent secretion of IL-10 (controlled by IRAKs 1 and 2) was only reduced mod

233 Significantly lower secretion of IL-10 and higher secretion of IL-9 by casein-stimulated

234 ISG15 also enhanced secretion of IL-10, indicating a broader role for ISG15 in cytokine s

235 hi phagocytosis, stimulation of secretion of IL-10.

236 However, the critical cellular source of IL-10 during M. tuberculosis infection is still unknown.

237 (Treg) cells were the predominant source of IL-10 in response to PGRN.

238 that uterine NK cells are the key source of IL-10 that is required to regulate DC phenotype and preg

239 -) CD14(+) monocytes were the main source of IL-10.

240 that, despite the multiple immune sources of IL-10 during M. tuberculosis infection, activated effect

241 cytokines and TLR-4 while increased that of IL-10 after LPS stimulation.

242 uld be abrogated by the adoptive transfer of IL-10(+/+) NK cells and not by IL-10(-/-) NK cells.

243 TR1 cell regulatory activity is dependent on IL-10 receptor signaling.

244 IM-mediated protection was dependent on IL-10, given that Il10(-/-) CpG-induced IMs lacked regul

245 d binding to putative responsive elements on IL-10 promoter.

246 secretion by B cells and CD1d expression on IL-10 secreting B cells was lower in VDR KO mice.

247 ents at the time of clinical presentation on IL-10 production and its association with S. aureus bact

248 c IL-2/Fc, nonlytic IL-2/Fc, TGF-beta/Fc, or IL-10/Fc fusion proteins to promote chimerism to induce

249 alpha, IL-12 p70, IL-17A, GM-CSF, IL-12 p40, IL-10, IL-7, IL-1alpha, and IL-5) subject-to-subject var

250 jections of plasmid DNA encoding IL-10 (pDNA-IL-10) into the NAc of non-handled rats.

251 In contrast, neither handling nor pDNA-IL-10 treatment alters self-administration of food or su

252 However, after day 21 postinfection, IL-10-expressing T cells were also highly represented.

253 ortantly, we show that treatment of pregnant IL-10(-/-) mice with A-1254 resulted in placental activa

254 These cells produce IL-10 and downregulate some pro-inflammatory genes.

255 cies of CD1d(hi) CD5(+) and IL-10-producing (IL-10(+)) CD45(+) cells were decreased.

256 educing the expression of CD86 and promoting IL-10.

257 Supporting these biological properties, IL-10-based modeling predicts two DNA-binding domains, t

258 signalling with CD40 ligation did not reduce IL-10 secretion as was observed in healthy control trans

259 idoglycan O-acetyltransferase mutant reduces IL-10, increases IL-1beta, and promotes development of I

260 ss-activated protein kinases (MSKs) regulate IL-10 production via the phosphorylation of cAMP respons

261 anscription factors that positively regulate IL-10 expression (MAFB, AhR), and promotes a proinflamma

262 cription factor ETS variant (Etv)5 regulates IL-10 production in Th2 cells.

263 that Etv5 plays a crucial role in regulating IL-10 production in Th2 cells by facilitating the bindin

264 ed systemic levels of type 2 and regulatory (IL-10 and TGF-beta) cytokines.

265 cells to cure diabetes in NOD mice required IL-10 signaling, as Tr1 cells could not suppress CD4(+)

266 ression in Th2 cells that lack Etv5 restored IL-10 production and the binding of IL-10-inducing trans

267 HLA class II-restricted IL-10 production by drug-specific T cells from exposed p

268 wever, while cytokine qPCR analysis revealed IL-10, IL-12, IL-13, IL-23 and TGFbeta were elevated, th

269 B was higher in patients with elevated serum IL-10 vs patients with low IL-10 (35.5 vs 0.5 median CFU

270 We found a significant increase in serum IL-10 and IL-8 levels after a positive OFC result.

271 liver injury models, we show that the STAT3-IL-10-IL-6 axis is a positive regulator of macrophage ef

272 We detected a decrease in the sustained IL-10 production by NK cells and lower serum levels of I

273 Here, we report a novel finding that IL-10 triggers a signal transducer and activator of tran

274 inhibitors and knockout mice, we found that IL-10 induction in B cells was regulated by an ERK1/2- a

275 In this study we report that IL-10 is essential for anti-Plasmodium humoral immunity.

276 Here, we report that IL-10 was rapidly induced following intestinal mucosal i

277 The data show that IL-10 secretion by B cells and CD1d expression on IL-10

278 Furthermore, the IL-10 expressing NK cells markedly enhanced angiogenic r

279 ent of CREB to its responsive element in the IL-10 promoter.

280 which is shared by multiple cytokines in the IL-10 superfamily.

281 SD exacerbates inflammatory pathology in the IL-10-deficient murine model of colitis relative to mice

282 IL-19, a member of the IL-10 cytokine family that signals through the IL-20 rec

283 IL-26 is a member of the IL-10 cytokine family, overexpressed in numerous chronic

284 Moreover, manipulation of the IL-10 signaling pathway represents a novel approach for

285 sponse element-binding (CREB) protein on the IL-10 promoter.

286 Here we investigate the impact on the IL-10-mediated anti-inflammatory response.

287 nt of a repressive NCOR/HDAC3 complex to the IL-10 promoter, but not the TNF promoter, thereby tippin

288 se data demonstrate that IL-4 contributes to IL-10 production and that Th2 cells modulate Th1 culture

289 s as a critical innate immune contributor to IL-10-induced wound closure.

290 The mechanisms leading to IL-10 expression by CD4(+) T cells are being elucidated,

291 l studies intravaginally infected wild-type, IL-10(-/-), IL-4(-/-), and IL-4Ralpha(-/-) mice with low

292 nrecognized signaling pathway that underlies IL-10 production by PGRN in Treg cells and present new i

293 ivotal transcription factor for upregulating IL-10 production by B-1a cells in sepsis through its nuc

294 Using IL-10 as an initial biomarker, clinicians may consider m

295 Using IL-10 reporter mice, we show in this article that during

296 ng expansion of the Treg cell population via IL-10.

297 In vitro, IL-10 expression was detected only when tendon cells wer

298 suppressive effects of NLRP3 signaling were IL-10 dependent.

299 d IL-23, but not IL-6 and TNF-alpha, whereas IL-10 levels were increased in peripheral blood of clini

300 n expression were significantly higher while IL-10 mRNA levels were lower in PI-IBS D than in HC in b

301 ssive inflammation and the mice treated with IL-10-deficient B-1a cells were not protected against se