ライフサイエンスコーパス: IL-10

1 IL-10 and IFN-gamma signaling were disrupted by using bl

2 IL-10 counterregulates IRF5 activation by GM-CSF.

3 IL-10 from effector T cells signals to CD11c(+) myeloid

4 IL-10 is a potent anti-inflammatory cytokine capable of

5 IL-10 promotes IL-10RB/ATG16L1 interaction through the W

6 IL-10 regulates T(H) cell phenotypes and can dampen T2 i

7 IL-10 was also inversely associated with total coronary

8 IL-10(+) CD4(+) T cells expressed the highest levels of

9 IL-10, a hallmark of PEL, was dependent on the IRAK path

10 IL-10-oriented posttransplant response was associated wi

11 IL-10-regulated genes are involved in monocyte energy ho

12 (CASP1), intercellular adhesion molecule 1, IL-10, heme oxygenase 1 hypoxia-inducible factor 1 (HIF-

13 ence-activated cell sorting; interleukin 10 (IL-10) and IL-18 and soluble FAS ligand (sFASL) were mea

14 rthermore, the expression of interleukin 10 (IL-10) at the RNA and protein levels was significantly i

15 genetic approaches inhibited interleukin 10 (IL-10) expression and increased expression of the p40 su

16 Interleukin 10 (IL-10) is an anti-inflammatory cytokine that may be prot

17 Interleukin 10 (IL-10) is an antiinflammatory cytokine, but also promote

18 ammatory cytokines including interleukin 10 (IL-10), IL-35 and transforming growth factor-beta.

19 IL-5), interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 22 (IL-22), and tumor necrosis facto

20 is the dramatic elevation of interleukin 10 (IL-10).

21 e anti-inflammatory cytokine interleukin-10 (IL-10) and the metalloproteinase MMP9.

22 we explored the role of the interleukin-10 (IL-10) axis in restoring murine microglia homeostasis fo

23 ells, the immune-suppressive interleukin-10 (IL-10) cytokine, and the down-modulatory tryptophan cata

24 including increased PD-1 and interleukin-10 (IL-10) expression by cytotoxic T cells in H5N1 (2:6)-inf

25 Interleukin-10 (IL-10) is a dimeric cytokine with both immunosuppressive

26 tion clones are deficient in interleukin-10 (IL-10) production.

27 e tissue macrophages produce interleukin-10 (IL-10) upon feeding, which suppresses hepatic glucose pr

28 sly shown that expression of Interleukin-10 (IL-10), a classical anti-inflammatory cytokine, extends

29 tumor necrosis factor alpha, interleukin-10 (IL-10), IL-12, IL-1alpha, IL-6, and IL-17.

30 sed production of TNF-alpha, IL-6, IL-12p70, IL-10, GM-CSF, VEGF, MIP-1beta, TNF-beta, IFN-alpha2 and

31 heniformis PGA elicited those plus IL-12p70, IL-10, IL-1beta, and TNF-alpha.

32 nal model of 6 biomarkers (CXCL10, IL-1beta, IL-10, sCD14, tumor necrosis factor [TNF]-alpha, and TNF

33 nflammation (IL-6, IFN-gamma, IP-10, IL-1RA, IL-10), chemotaxis (IL-8), systemic and vascular inflamm

34 ytokines involved in tissue repair (PGE(2) , IL-10) generally impaired by frequently used corticoster

35 0 elicitors revealed that IL-2, IL-4, IL-27, IL-10, and neuromedin U (NMU) increased IL-10 production

36 interleukin-12 [IL-12], IL-23, IL-6, IL-27, IL-10, transforming growth factor-beta) that expand and

37 F-alpha (ratio 2.05), IL-1beta (ratio 1.45), IL-10 (ratio 1.97), while CCL22 (ratio 0.65) was downreg

38 duction of the cytokines interleukin (IL)-6, IL-10, transforming growth factor beta (TGF-beta), and i

39 e of IFN-gamma, TNF-alpha, IL-2, IL-4, IL-6, IL-10 and IL-17A from isolated, stimulated T cells of 27

40 DHF had significantly higher levels of IL-6, IL-10 and MIP3alpha than those who developed mild illnes

41 ine production in lungs including TNF, IL-6, IL-10, and IFN-gamma.

42 Other cytokines examined, such as IL-6, IL-10, and monocyte chemotactic protein-1, showed no con

43 e were no overall differences in serum IL-6, IL-10, C-reactive protein, and length of stay.

44 Plasma and BAL IL-4, IL-6, IL-10, IL-13 and TNF-alpha correlated with BAL fungal pr

45 nt dysregulation of IFN-gamma, IL-1RA, IL-6, IL-10, IL-19, monocyte chemoattractant protein (MCP)-1,

46 , 0.93, 0.99, 0.96, and 0.75 for IL-5, IL-6, IL-10, IL-22, and TNFalpha, respectively.

47 lammatory response (elevated IL-1beta, IL-6, IL-10, IL-8, RANTES, and TNFalpha) while the response to

48 t form has been marked by elevation of IL-6, IL-10, TNF-alpha, and other cytokines and severe CD4(+)

49 ess.Methods: Levels of IL-1beta, IL-6, IL-8, IL-10, and sTNFR1 (soluble tumor necrosis factor recepto

50 and IgG), and cytokine content (IL-6, IL-8, IL-10, and TNF-alpha), and antioxidant activity of human

51 gnificantly increased (IL-1beta, IL-6, IL-8, IL-10, and TNF-alpha).

52 s of IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, CRP, TNF-alpha, IFN-gamma, GM-CSF, MIP-1al

53 n values for interleukin (IL)-4, IL-6, IL-8, IL-10, IL-15, granulocyte colony-stimulating factor (GCS

54 of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-17, interferon-gamma and differential T and B

55 nel of five cytokine biomarkers (IL-6, IL-8, IL-10, TRAIL & IP-10), that is attributed as a sign of t

56 L-1beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-10, IL-12(p40), IL-13, IL-17, CCL2, CCL3, CCL4, CCL5,

57 Interestingly neither AAV-M3 alone nor AAV-IL-10 + AAV-M3 extend survival beyond that of the AAV-IL

58 AV-M3 extend survival beyond that of the AAV-IL-10 alone cohort.

59 thelial barrier to focus biologically active IL-10 to the intestinal lamina propria.

60 Both IL-1beta/IL-1Ra and TNF-alpha/IL-10 ratio in Candida hyphae-stimulated PBMCs were sign

61 Although IL-10 levels were significantly higher in COVID-19 patie

62 reveal a hitherto unappreciated role for an IL-10-STAT3-Blimp-1 circuit as an initiator of an inflam

63 We generated an IL-10 mutant with enhanced affinity for its IL-10Rbeta r

64 IL-1alpha (P <0.05), IL-1beta (P <0.001) and IL-10 (P <0.01) compared with the periodontitis group.

65 expression of programmed death-ligand 1 and IL-10, and decreased expression of interferon-gamma.

66 Thus, both IL-4/13 and IL-10 paralogs in zebrafish exhibit aspects of conserved

67 amma, IFN-beta, IFN-lambda, IL-4, IL-13, and IL-10 cytokines to better understand the heterogeneity o

68 ys 1, 3, and 7 were assayed for IL-1beta and IL-10 by enzyme-linked immunosorbent assay and compared

69 Regarding treatment groups, IL-1beta and IL-10 were similar prior to receiving antibiotic.

70 han the anti-inflammatory cytokines IL-4 and IL-10 in tonsil and blood samples in RAT, PTA, and sampl

71 T cell mediated Leishmania-specific IL-4 and IL-10 responses, and consequently with high pro/anti-inf

72 miR-147 inhibited the production of IL-6 and IL-10 and significantly reduced M. marinum intracellular

73 and associated aqueous or vitreous IL-6 and IL-10 levels were collected retrospectively.

74 IL-6 and IL-10 were not affected by any of the treatments applied

75 es anchored by interleukin (IL)-4, IL-6, and IL-10 demonstrated greatest rewiring, while in hyperglyc

76 dimer, B-type natriuretic peptide, IL-6, and IL-10 levels were common but not ubiquitous.

77 IgE responses, whereas IFN-gamma, IL-6, and IL-10 were dispensable.

78 y cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected early after P. yoeli

79 icantly higher levels of IL-1beta, IL-6, and IL-10, likely overcoming any protective effects that mig

80 ry cytokines (e.g., interleukin-6 [IL-6] and IL-10), in mycobacterial infection.

81 Low levels of TNF-alpha and IL-10 and high levels of CCL22 predicted better treatmen

82 nd a higher gene expression of TNF-alpha and IL-10 at 45I-120R.

83 We found that TNF-alpha and IL-10 control optimal CXCL13 gene expression in MoDM and

84 TNF-alpha and IL-10 discriminated between patients with MIS-C and seve

85 , IL-1beta, tumor necrosis factor-alpha, and IL-10 and lower levels of IL-2 were observed in CDC pati

86 ymptoms, and levels of TNF-alpha, CCL22, and IL-10 may predict the response to azithromycin treatment

87 khead box P3-positive regulatory T cells and IL-10(+) and TGF-beta1(+) skin-resident macrophages.

88 ct was on the reduction of Th2 cytokines and IL-10 in PBMC cultures.

89 spase-1 were all significantly decreased and IL-10 was increased with both combinations.

90 nctions expression in human enterocytes, and IL-10, IFN-gamma and FoxP3 expression through epigenetic

91 of exosomes isolated from wild-type EPC and IL-10 knockout EPC.

92 s revealed wild-type EPC-derived exosome and IL-10 knockout EPC-derived exosome contain different pro

93 ndent forkhead box P3 (Foxp3) expression and IL-10 production.

94 cells, using activation markers, FoxP3, and IL-10 expression.

95 T(FR) and IL-10(+) cT(FH) cells were induced in SCIT and SLIT grou

96 bserved impaired production of IFN-gamma and IL-10 by whole blood from beta-thalassaemia patients upo

97 in vitro reduced production of IFN-gamma and IL-10 from healthy human PBMCs and decreased bacterial c

98 glomerations, characterized by IFN-gamma and IL-10 phenotypes, respectively.

99 ll reservoir via regulation of IFN-gamma and IL-10.

100 nes such as TNF-alpha, IL-12, IFN-gamma, and IL-10 in immunity and pathogenesis to the blood stage ma

101 Interleukin 6 levels were higher and IL-10 levels were lower in uveitis patients compared wit

102 IL-6, keratinocyte chemoattractant [KC], and IL-10) were measured in nasal washes and middle ear tiss

103 I contains elevated amounts of D-lactate and IL-10 compared with control subjects, and bacterial lact

104 age counts, potentiating the macrophage- and IL-10-associated mechanisms of joint homeostasis lost du

105 inhibition of Malat1 also suppresses Maf and IL-10 levels.

106 expression of purinergic receptors MMP9 and IL-10 is reduced.

107 T) mice and transfer of IL-10-proficient and IL-10-deficient B cells to muMT mice.

108 egulated by transfer of IL-10-proficient and IL-10-deficient B cells.

109 logistic regression model, ISOLD score, and IL-10-to-IL-6 ratio achieved AUCs of 98.3%, 97.7%, and 9

110 L-12 (p70), tumor necrosis factor (TNF), and IL-10, was observed in mice after S. suis type 2 infecti

111 0RB/ATG16L1 interaction through the WDD, and IL-10 signaling is suboptimal in cells lacking the WDD o

112 Anti-IL-10-treated nonhuman primates had similar overall dise

113 Interestingly, IL-12 and anti-IL-10 Abs improved T cell proliferation inhibited by AmB

114 nges in granulomas and lymph nodes from anti-IL-10-treated animals.

115 xygen species and augmented antiinflammatory IL-10 production both in vitro and in LPS-challenged mic

116 cted between IL-10 levels and the CTII area, IL-10 and the percentage of Syndecan, and the area of CT

117 ects of anti-inflammatory cytokines, such as IL-10, in TB are less well understood.

118 ely, whereas H3K4 trimethylation by Ash1l at IL-10 promoter induced its expression.

119 ncluding IDO-1, arginase-1, Foxp3, TGF-beta, IL-10, and decreased levels of proinflammatory T-bet, IL

120 significant correlation was detected between IL-10 levels and the CTII area, IL-10 and the percentage

121 ts identify a regulatory interaction between IL-10 and PGE2, dysregulation of which may drive aberran

122 ) and increased splenic Tregs producing both IL-10 and IFN-gamma 8-fold (p < 0.005) compared to LL-ve

123 ponse in the pretransplant group replaced by IL-10-dominated response in the 1-6 m posttransplant gro

124 of CAC, we show that the LRP5/6-beta-catenin-IL-10 signaling axis in intestinal CD11c(+) APCs protect

125 om the MLNs of GIARS mice were mostly CCL1(+)IL-10(+)LIGHT(+)miR-27a(+) M (M2bM , inhibitor cells for

126 tudy on the alteration by pLL of CD86, CD40, IL-10, and IL-12 responses to LPS in BMDC; however, we n

127 In vivo, the reduced CD4(+) T cell IL-10 expression in Malat1(-/-) mice underpins enhanced

128 Delta9-THC-induced early rise in circulating IL-10.

129 Conclusions: IL-10 deficiency/inflammation alters EPC-derived exosome

130 n wild-type, IL-10 reporter, and conditional IL-10 or IL-10 receptor alpha (IL-10Ralpha) knockout mic

131 iciency virus (PWH) and uninfected controls, IL-10 was measured in serum samples by means of enzyme-l

132 s of EGF (epithelial growth factor), GM-CSF, IL-10, CCL2/MCP-1, CCL3/MIP-1a, CXCL10/IP-10, CCL5/RANTE

133 is mediated by the immunoregulatory cytokine IL-10.

134 expression of the immunosuppressive cytokine IL-10.

135 Surprisingly, the anti-inflammatory cytokine IL-10, but not the pro-inflammatory cytokines IL-6 or IL

136 eptor to increase expression of the cytokine IL-10.

137 ed levels of the anti-inflammatory cytokine, IL-10 were observed in the hippocampus during chronic DS

138 xpression of the anti-inflammatory cytokine, IL-10, in T(H)17 cells.

139 y cells, and the anti-inflammatory cytokine, IL-10, that antagonizes both innate and acquired immune

140 The cytokines IL-10, IL-13, IL-4, and IL-1alpha were negatively associ

141 with suppression of two major Th2 cytokines, IL-10 and IL-13.

142 S, significantly increased TNF and decreased IL-10 production in DCs.

143 GSK3, which in turn promote BLIMP1-dependent IL-10 production.

144 Ablation of T cell-derived IL-10 increased the IFN-gamma and IL-17A response to HDM

145 uced production of adaptive immunity-derived IL-10 and, in turn, increased activation of macrophages.

146 At nonsaturating doses, IL-10 did not induce key components of its gene expressi

147 3) production of anti-inflammatory effectors IL-10 and thioredoxin 1.

148 NTs are the most sensitive markers; elevated IL-10 and IL-18 are additional indicators for ALPS.

149 monocytes, but B. subtilis PGA also elicited IL-10 and TNF-alpha, whereas B. licheniformis PGA elicit

150 Our engineered IL-10 variant showed a more robust bioactivity profile t

151 odified T cells expanded with the engineered IL-10 variant displayed superior cytolytic activity than

152 he wild-type cytokine, the affinity-enhanced IL-10 variants recruited IL-10Rbeta more efficiently int

153 nstream diurnal activity of intra-epithelial IL-10(+) lymphocytes regulating the SI barrier function.

154 Of the cytokines evaluated, IL-10 was significantly higher (p < 0.0001) in those who

155 (Danio rerio) and, together with an existing IL-10 mutant line, characterized the consequences of los

156 atory cytokines in the presence of exogenous IL-10.

157 CD4(+)CCR6(+)T cells expressing IL-10, but not IL-17, were also detectable in the spleen

158 in presymptomatic SOD1-G93A mice expressing IL-10 + M3 or IL-10 alone.

159 and up-regulate an anti-inflammatory factor (IL-10) in inflamed Raw 264.7 cells.

160 opens new opportunities to revitalize failed IL-10 therapies.

161 Finally, IL-10 neutralization abolished the protective effects of

162 lic dependency on the glycolytic pathway for IL-10 production, shifting from the fatty acid oxidation

163 F3 is associated with but not sufficient for IL-10 expression in CD4(+) T cells.

164 whereas the numbers of FoxP3(+) and FoxP3(-) IL-10-secreting regulatory T cells were reduced.

165 -purified populations of both low-frequency (IL-10(+); GM-CSF(+)) and high-frequency (TNF(+)) cytokin

166 At 8 wk postinfection, lung granulomas from IL-10-neutralized animals had reduced cytokine productio

167 tion in lung granulomas and lymph nodes from IL-10-neutralized animals at 3-4 wk postinfection compar

168 Five cytokines (IFN-gamma, IL-10, IL-6, IL-8, and TNF-alpha) contributed to the ana

169 Higher production of IL-17A, IFN-gamma, IL-10, IP-10, GM-CSF, sFasL, Granzyme A, Granzyme B, Gra

170 h anti-inflammatory responses including high IL-10:IL-6 and kynurenine to tryptophan ratios show less

171 We sought to determine how IL-10 regulates the balance of T(H) cell responses to in

172 to this pleiotropic cytokine, including how IL-10 regulates basic processes of neural and adipose ce

173 Our study provides insights into how IL-10 receptor complex stability fine-tunes IL-10 biolog

174 e and immunostimulatory activities; however, IL-10-based therapies have shown only marginal clinical

175 Clinical use of human IL-10 (hIL-10) has been limited by anemia and thrombocyt

176 pathway for the optimal functioning of human IL-10 producing regulatory B cells.

177 Foxp3(+) and Foxp3(-) PD1(+) CD73(+) ICOS(+) IL-10(+) peripheral regulatory T cells in prediabetic mi

178 rs including IL-6, CXCL10, CXCL11, IFNgamma, IL-10, and monocyte-attracting CCL2, CCL7 and CCL8, was

179 nally regulated diet-microbiome-MHC class II-IL-10-epithelial barrier axis by circadian clock disarra

180 RS-CoV2 and high levels of immunosuppressive IL-10 in both COVID-19 and dengue during early illness a

181 Among PWH, a 10-fold decrease in IL-10 was associated with a 2.6-fold increase in the odd

182 he activation marker CD86 and an increase in IL-10 production and was associated with a higher prolif

183 Intriguingly, ILK knockdown in IL-10 knockout EPC-derived exosome significantly rescued

184 , which led to decreased H3K4 methylation in IL-10 gene locus.

185 nical pathways in patients with VOC included IL-10 signaling, iNOS signaling, IL-6 signaling, and B c

186 immunomodulatory one, as shown by increased IL-10 production by monocytes.

187 -27, IL-10, and neuromedin U (NMU) increased IL-10 production in activated intestinal ILC2s, while TL

188 ession in activated T cells led to increased IL-10 expression and a decrease in the expression of IFN

189 ol subjects, and bacterial lactate increases IL-10 production by human monocyte-derived macrophages.

190 concentrations and progressively increasing IL-10 and IGF-1 concentrations.

191 s screened for mutants that failed to induce IL-10 in myeloid-derived suppressor cells (MDSCs), which

192 -12 induced by LPS, whereas only AmB induced IL-10 secretion; both cytokines are essential in regulat

193 agonistic peptide restores IL-12 and induces IL-10 expression by DCs treated with lipocalin allergens

194 ts indicate that Delta9-THC potently induces IL-10, while reducing proinflammatory cytokines, chemoki

195 ens, attenuating the T(H)2 bias and inducing IL-10 production in cocultured T(H) cells.

196 expansion of peripheral and CNS-infiltrating IL-10(+) T cells.

197 The expression of anti-inflammatory IL-10 by CD4(+) T cells is indispensable for immune home

198 lockade of ERK signaling similarly inhibited IL-10 expression but decreased IL-12/23p40 expression, w

199 istically, butyrate induced small intestinal IL-10 expression and downregulated the claudin-2 express

200 ion of Tfr cells for IgE production involves IL-10, and the loss of IL-10 signaling by B cells led to

201 The avirulent strain induced less IL-10, but higher IL-12, in macrophages.

202 2 mutant biofilm produced substantially less IL-10 compared with wild-type S. aureus, which was also

203 It is known that host leukocyte IL-10 production is required for S. aureus biofilm persi

204 vels of IL-1beta, IL-6, and sTNFR1 but lower IL-10 than CAP(ICU) patients.

205 lation/demethylation of M(LPS + IFN-gamma)/M(IL-10) genes is one of the factors that direct macrophag

206 that through promoting expression of the Maf/IL-10 axis in effector Th cells, Malat1 is a nonredundan

207 As in mammals, IL-10 appears to have a more striking anti-inflammatory

208 Regulatory T-cell-related mediators (IL-10 and FOXP3) were comparably upregulated in all grou

209 ighlight the critical role of non-microglial IL-10 in preventing deleterious microglia hyperactivatio

210 discover that the microglial IL-10 receptor counteracts the pro-inflammatory effects

211 Mycobacterium tuberculosis and secreted more IL-10.

212 Disruption of the T cell-myeloid IL-10 axis resulted in increased pulmonary monocyte-deri

213 e role of IL-10, we used an Ab to neutralize IL-10 in cynomolgus macaques during M. tuberculosis infe

214 doptive transfer of IL-10-proficient but not IL-10-deficient B cells into muMT mice before HDM-sensit

215 at early changes occurring in the absence of IL-10 may lead to better bacterial control later during

216 ed IL-13/IL-17A response and accumulation of IL-10-producing forkhead box P3-negative effector CD4(+)

217 n CD11c(+) APCs or in vivo administration of IL-10 protected LRP5/6(DeltaCD11c) mice from CAC by supp

218 may help develop an effective application of IL-10 in diverse clinical settings.

219 ion was restricted by high concentrations of IL-10.CONCLUSIONThis study demonstrates the induction of

220 ets provide insight into the contribution of IL-10 to the immunological balance necessary for granulo

221 ponse, characterized by increasing counts of IL-10(+) macrophages, decreasing IL-1beta concentrations

222 Augmented expression of IL-10, a critical anti-inflammatory cytokine, in turn, a

223 ssociated virus (AAV)-mediated expression of IL-10, alone, or in combination with M3, resulted in mod

224 es showed significantly higher expression of IL-10, TLR4, high-mobility group box 1, IFN-gamma, TRIF-

225 for anti-CD3/CD28 mAb-mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.

226 1 and Th17 cytokines as well as induction of IL-10.

227 charide stimulation and optimal induction of IL-10.

228 Additionally, the level of IL-10 in activated T cells was low when the expression o

229 Levels of IL-10, IL-6, and matrix metalloproteinase-2 were signifi

230 E production involves IL-10, and the loss of IL-10 signaling by B cells led to a severely curtailed p

231 Loss of IL-10 signaling in macrophages (Mphis) leads to inflamma

232 Objective: To determine the mechanisms of IL-10 (interleukin-10) deficient-EPC-derived exosome dys

233 In contrast, null mutation of IL-10 diminished M2-biased macrophages but produced no d

234 ntributes to the immunomodulatory potency of IL-10.

235 mediated primarily through the production of IL-10.

236 l spherocytosis and macrophage production of IL-10.

237 r current understanding of the regulation of IL-10 production and of the molecular pathways associate

238 n of Maf, a key transcriptional regulator of IL-10 Maf expression correlates with Malat1 in single Ag

239 that IKZF3 is a transcriptional regulator of IL-10 using a human CD4(+) T cell-only culture system.

240 To investigate the role of IL-10, we used an Ab to neutralize IL-10 in cynomolgus m

241 ytoprotection for CEnCs through secretion of IL-10, indicating potentially novel therapeutic targets

242 ummary, ILC2s provide an inducible source of IL-10 in the gastrointestinal tract, whereas ILCregs are

243 that AW112010 regulated the transcription of IL-10.

244 , a murine model of MS, adoptive transfer of IL-10(+) regulatory B cells (B(regs)) has been shown to

245 B-cell-deficient (muMT) mice and transfer of IL-10-proficient and IL-10-deficient B cells to muMT mic

246 ells were equally upregulated by transfer of IL-10-proficient and IL-10-deficient B cells.

247 Adoptive transfer of IL-10-proficient but not IL-10-deficient B cells into mu

248 n (IL)-1beta (P = .050), and upregulation of IL-10 (P < .047) and Indolamine-2, 3-dioxygenase (P = .0

249 pe, IL-10 reporter, and conditional IL-10 or IL-10 receptor alpha (IL-10Ralpha) knockout mice by mean

250 Adjuvant removal, B cell depletion, or IL-10 blockade recovers its antitumor effectiveness.

251 atic SOD1-G93A mice expressing IL-10 + M3 or IL-10 alone.

252 d volunteers, norepinephrine enhanced plasma IL-10 concentrations and attenuated the release of the p

253 On presentation, IL-10 was elevated in mortality (P = .008) and persisten

254 of ILC2s in the lungs that actively produce IL-10 (ILC2(10)s).

255 rophages and stimulated the cells to produce IL-10, TGF-beta, or both at the immunization site, which

256 scribe IL-10 mRNA and, accordingly, produced IL-10 upon primary activation.

257 low percentage of intestinal ILC2s produced IL-10 at steady state.

258 )IL-7R(+)T cells from human tonsils produced IL-10 following stimulation by naive B cells, which prom

259 afollicular B helper T cells, which produced IL-10 and could play a prominent pathogenic role in SLE.

260 T cell subset that is committed to producing IL-10.

261 suggest that dramatic early proinflammatory IL-10 elevation may play a pathological role in COVID-19

262 A screen for putative IL-10 elicitors revealed that IL-2, IL-4, IL-27, IL-10,

263 in the gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-beta and GITR; P < 0.05), and the proliferati

264 he IRAK pathway, as IRAK4 KOs showed reduced IL-10 levels.

265 nscription factors cMaf and Blimp-1 regulate IL-10 expression in ILC2(10)s.

266 Mechanistically, Malat1 regulates IL-10 through enhancing expression of Maf, a key transcr

267 Serum IL-10 and IL-6 were significantly elevated at presentati

268 Levels of serum IL-10 (p = 0.0001), IL-6 (p = 0.002), MIP-3alpha (p = 0.

269 Since IL-10 suppresses T cell function, this suggests that the

270 Strikingly, IL-10-producing CCR6(+)T cells were highly abundant in l

271 Stronger IL-10 responses were found following complicated appendi

272 ated intestinal ILC2s, while TL1A suppressed IL-10 production.

273 ments with IL-10(-/-) mice demonstrated that IL-10 was not required for protection against anaphylaxi

274 expression increased microglial burden, the IL-10 + M3 group showed lower microglial burden, suggest

275 ; and 94.2%, 95.3%, 95.6%, and 93.9% for the IL-10-to-IL-6 ratio.

276 re, we explored whether the stability of the IL-10 receptor complex contributes to the immunomodulato

277 C-peptide levels in the period preceding the IL-10 response, but stable graft function following the

278 pha1) and the common IL-10R2, belongs to the IL-10 cytokine family, and is critically involved in tis

279 Recipients within the IL-10(+) cluster had a significant decline in C-peptide

280 In addition to IL-10's classic inhibitory effects on myeloid cells, we

281 cytokine stimulation but did not respond to IL-10.

282 n 13 (IL-13)] and T regulatory type-1 (Tr1) (IL-10) response when LN cells were challenged with Ova i

283 ells were found to constitutively transcribe IL-10 mRNA and, accordingly, produced IL-10 upon primary

284 IL-10 receptor complex stability fine-tunes IL-10 biology and opens new opportunities to revitalize

285 t bioactivity profile than that of wild-type IL-10 at low doses in monocytes and CD8(+) T cells.

286 activity than those expanded with wild-type IL-10.

287 gic airway disease was induced in wild-type, IL-10 reporter, and conditional IL-10 or IL-10 receptor

288 expression of IKZF3 was unable to upregulate IL-10 at the mRNA or protein level in CD4(+) T cells and

289 ression, and cytokine secretion, upregulated IL-10 secretion, and inhibited Phl p 5-induced basophil

290 Finally, using IL-10-GFP reporter mice, we showed that blood monocytic

291 Methods and Results: Using IL-10 knockout mice mimicking systemic inflammation cond

292 cell transcriptome analysis revealed various IL-10 producing immune cells in the CNS, including most

293 tion of IL-10 but is dispensable for ex vivo IL-10 expression.

294 promoted post-MI neovascularization, whereas IL-10 knockout EPC-derived exosome treatment showed dimi

295 Further, while IL-10 expression increased microglial burden, the IL-10

296 nd of the molecular pathways associated with IL-10 responses.

297 h ex vivo and after activation compared with IL-10-CD4(+) T cells.

298 In mammals, IL-4 and IL-13 in concert with IL-10 are essential for balancing immune responses to pa

299 concentration was positively correlated with IL-10 and negatively correlated with concentrations of M

300 sigmodontis infection, and experiments with IL-10(-/-) mice demonstrated that IL-10 was not required