ライフサイエンスコーパス: IL-12

1 IL-12 family members IL-12p70 and IL-23 are important fo

2 IL-12 is composed of two different subunits, p40 and p35

3 IL-12 plays a critical role in the early inflammatory re

4 while cytokine qPCR analysis revealed IL-10, IL-12, IL-13, IL-23 and TGFbeta were elevated, these wer

5 rleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, IL-12, interferon gamma, tumor necrosis factor alpha, an

6 Four additional analytes (IP-10, IL-12/23p40, IFNy, IL-15) were found to be elevated in H

7 vo in D6(+/+) mice (2-fold increase in IL-10/IL-12 ratio) but not their D6(-/-) counterparts.

8 Interleukin 12 (IL-12) and IL-18 regulated this conversion, and during v

9 he proinflammatory cytokines interleukin 12 (IL-12) and IL-23 connect innate responses and adaptive i

10 lular hematopoietic cytokine interleukin 12 (IL-12) in HCMV-infected cells but not in mock-infected c

11 hat treatment with exogenous interleukin 12 (IL-12) protects against F. tularensis infection; this pr

12 nization) is increased in an interleukin 12 (IL-12)-dependent manner.

13 racterize heparin binding to interleukin-12 (IL-12) and determine the mechanism(s) by which heparin i

14 t but not following combined interleukin-12 (IL-12) and IL-18 stimulation.

15 he significant production of interleukin-12 (IL-12) and IL-6.

16 Interleukin-12 (IL-12) has emerged as one of the most potent agents for

17 on and the downregulation of interleukin-12 (IL-12) p40 mRNA were correlated with the dose of LP-BM5

18 ors in STAT4, which controls interleukin-12 (IL-12) responses, have not yet been reported.

19 /CXCL9, and severe defect of interleukin-12 (IL-12) secretion.

20 body-based neutralization of interleukin-12 (IL-12), but not IL-10, produced by M1 macrophages also a

21 r synergistic stimulation of Interluekin-12 (IL-12) production when the TLR signaling intensity is lo

22 Transcript levels of IL-12p35, IL-12/23p40 and IL-23p19 were measured using RT-PCR.

23 ated NK cells with cytokines, such as IL-15, IL-12, or IL-18, does not activate LFA-1 but increases t

24 s with antibodies targeting IL-17A, IL-17RA, IL-12/23p40, or IL-23p19.

25 imulating factor (G-CSF), interleukin-12/23 (IL-12/23), and IL-13 trended significantly higher in SIV

26 of pro-inflammatory cytokines, such as IL-6, IL-12, and CCL2.

27 cretion of pro-inflammatory cytokines (IL-6, IL-12, and TNF-alpha) from macrophages was significantly

28 tant, but the late-phase production of IL-6, IL-12, and TNFalpha (controlled only by the pseudokinase

29 , EDN-1 and pro-inflammatory cytokines IL-6, IL-12, and TNFalpha.

30 -type natriuretic peptide), TNF-alpha, IL-6, IL-12, IL-17, malondialdehyde, and fetuin-a.

31 including tumor necrosis factor (TNF), IL-6, IL-12, IL-23, and IL-1beta.

32 ory cytokines in the serum (TNF-alpha, IL-6, IL-12, TGF-beta, and VEGF) were down regulated by DMDD.

33 d gene 3) is an important member of the IL-6/IL-12 cytokine family.

34 proinflammatory cytokines (IL-1alpha, IL-8, IL-12(p70)) and increased IP-10.

35 a show that nonfunctional box motifs abolish IL-12- and IL-23-induced STAT3 phosphorylation and cytok

36 In addition, IL-12 induced exosomes are able to strengthen the effect

37 infection or upon exogenous administration, IL-12 is sufficient to elicit the emergence of a populat

38 by hPDL cells significantly increased after IL-12 treatment.

39 gamma) were performed spontaneously or after IL-12 plus IL-18 stimulation in the presence of K562 or

40 owed that a group of three proteins (Apo AI, IL-12 and stem cell factor) yielded accuracy of 81.3%, s

41 d IL-10 while CD1(-) cDC secreted IFN-alpha, IL-12 and TNF-alpha.

42 L-6, and IL-1beta) or low (IL-15, TNF-alpha, IL-12 p70, IL-17A, GM-CSF, IL-12 p40, IL-10, IL-7, IL-1a

43 cretion of inflammatory cytokines TNF-alpha, IL-12, and IL-6; this effect was blocked by TGF-betaR1 i

44 ated by upregulation of IL-1beta, TNF-alpha, IL-12, and inducible nitric oxide synthase 2 and downreg

45 AC significantly reduced TLR4-stimulated AMo IL-12 production, relative to either treatment alone, an

46 Interleukin-23 (IL-23), an IL-12 family cytokine, plays pivotal roles in pro-inflam

47 Our data reveal an IL-12-driven hard-wired pathway of emergency NK-cell lym

48 th increased T-bet expression induced via an IL-12-dependent mechanism.

49 tion of patients and treatment with IL-1 and IL-12 receptor subunit beta 1 (Rb1) antibodies may also

50 High levels of IL-10 and IL-12/23p40 were significantly associated with amyloid d

51 terleukin-1beta (IL-1beta), IL-6, IL-10, and IL-12 by monocytes from human peripheral blood mononucle

52 tokine TNF-alpha, IL-1beta, IL-6, IL-10, and IL-12 production in human monocytes.

53 ors, including TNF, CCL5, CXCL10, IL-18, and IL-12 p40, and identified 140 drugs targeting 16 of them

54 There was increased IL-2 and IL-12 and reduced IL-4 immunostaining in VUE lesions.

55 ifferentiation that is regulated by IL-2 and IL-12 signaling and the combined activities of the trans

56 ffect of interleukins (ILs) such as IL-2 and IL-12 was evaluated in a separate study group by adminis

57 d the serum levels of Th1 cytokines IL-2 and IL-12, and Th2 cytokines IL-4 and IL-10, particularly du

58 rotein 65 Ag and combined exogenous IL-2 and IL-12.

59 , they have low IFN-gamma, IL-17F, IL-2, and IL-12 levels, with increased IL-10 production and NO syn

60 propose a mechanistic paradigm for IL-23 and IL-12 whereby cognate receptor binding to the helical cy

61 mal model of MS) in the absence of IL-23 and IL-12, respectively.

62 IL-12p35, IL-23p19, and IL-12/IL-23p40 knockout mice on a C3H/HeN background, su

63 n the production of IL-6 (0.80 vs. 2.33) and IL-12 (0.25 vs. 1.67).

64 and ELISA and a multiplex kit for IL-35 and IL-12, respectively.

65 une diseases.IL-12p35 is common to IL-35 and IL-12, which have opposing effects on inflammation.

66 flammatory role that members of the IL-6 and IL-12 cytokine families play in GVHD biology.

67 inflammatory cytokines, TNF-alpha, IL-6, and IL-12 (>10-fold of control) and AdipoR levels.

68 oinflammatory cytokines TNF-alpha, IL-6, and IL-12.

69 alpha [TNF-alpha], interleukin-6 [IL-6], and IL-12), anti-inflammatory cytokine (IL-10), and chemokin

70 hi) monocytes were involved in TNF-alpha and IL-12 production, whereas Ly6C(lo)TLR2(hi) monocytes wer

71 sed to M. bovis showed reduced TNF-alpha and IL-12, suggesting that the results found in mice can be

72 pe II interferon (IFN-gamma), TNF-alpha, and IL-12 in myeloid dendritic cells are of importance in ge

73 otective cytokines IFN-gamma, TNF-alpha, and IL-12, as well as recruitment of NK cells, CD11b(+), and

74 ron (IFN-gamma)-producing NK1.1(+) cells and IL-12.

75 IL12A mRNA expression and IL-12 and IL-35 protein levels were assessed by using qu

76 d potently induced Th1-biasing IFN-gamma and IL-12 in human blood, but lower levels of the proinflamm

77 onclusion, by its secretion of IFN-gamma and IL-12, M1, but not M0 or M2, was demonstrated to inhibit

78 y cytokines IL-1beta, TNFalpha, INFgamma and IL-12 p70 were significantly decreased in LPS-treated kn

79 p16 on cyclin-dependent kinase 4 levels and IL-12 secretion by DC.

80 l macrophages express high levels of TNF and IL-12 but low levels of peroxisome proliferator-activate

81 n with RSG reduces the expression of TNF and IL-12 in decidual macrophages from women who underwent s

82 decrease) and significantly reduced TNF and IL-12 levels in gingival tissues.

83 decrease) and significantly reduced TNF and IL-12 levels in the gingival tissues.

84 e products (TsSPs) that suppress---- TNF and IL-12 secretion from LPS-activated human dendritic cells

85 a, but were poor producers of IL-6, TNF, and IL-12, which are critical mediators of host protection.

86 ILC2 activation and plasticity in vivo, and IL-12 acted as the switch that determined an ILC2-versus

87 sfolding also occurs for IL-23alpha, another IL-12 family protein.

88 In this article, we show that IL-27, another IL-12 family member, is produced by myeloid cells in res

89 entation index were improved only after anti-IL-12/23 treatment and correlated with changes in global

90 patients were randomized to receive an anti-IL-12/23 (ustekinumab, n=50), anti-tumor necrosis factor

91 Anti-IL-17 and anti-IL-12/-23 regimens appear particularly effective in psor

92 d with anti-TNF-alpha and cyclosporine, anti-IL-12/23 treatment resulted in a greater improvement of

93 Although cytokines, such as IL-12 and IL-23, have been shown to shape plasticity of

94 cretion of proinflammatory cytokines such as IL-12, IL-6, or TNF-alpha, all of which are implicated i

95 release of proinflammatory cytokines such as IL-12, repress differentiation of naive CD4(+) T cells t

96 cells respond to signal 3 cytokines such as IL-12.

97 ion of STAT3 to regulate the balance between IL-12/IL-23 subunits causing a cytokine milieu rich in I

98 ial stimuli to induce secretion of bioactive IL-12 by DCs.

99 CXCR3-dependent manner, by NK cell-boosted, IL-12-, and CXCL9-producing XCR1(+) DCs.

100 enous IL-12 expression was induced, and both IL-12 and IFN-gamma remained elevated during the entire

101 receptor complexes mediated by IL-23, and by IL-12 family members in general, have remained elusive.

102 transient innate activation characterized by IL-12 production and upregulated costimulatory and lymph

103 ecific manner but are largely contributed by IL-12 and IL-18; v) as MAIT cells are primed by SAgs, th

104 or lacking ligands for SFRs were enhanced by IL-12 but suppressed by type I interferon.

105 interleukin (IL)-12/23p40 subunit shared by IL-12 and IL-23.

106 oregulatory activities of other single chain IL-12 subunits might be exploited to treat other autoimm

107 Combining IL-12/IL-23 blockade and acitretin may constitute an eff

108 consists of the unique IL-23R and the common IL-12 receptor beta1 (IL-12Rbeta1).

109 f HSCs plus CD4(+) cell recipients contained IL-12-secreting CD11c(+) cells and IFN-gamma-expressing

110 IL-15, TNF-alpha, IL-12 p70, IL-17A, GM-CSF, IL-12 p40, IL-10, IL-7, IL-1alpha, and IL-5) subject-to-

111 pment driven by the proinflammatory cytokine IL-12, which can occur independently of gammac-signallin

112 s was evident when the third signal cytokine IL-12 was added, which also affected cytomegalovirus- an

113 AT5 upregulated the Th1-stimulatory cytokine IL-12 in classically activated macrophages, whereas in a

114 RNA-mediated down-regulation of the cytokine IL-12 decreases the recognition of infected cells by EBV

115 ing the levels of pro-inflammatory cytokines IL-12 and TNF-alpha.

116 ng nonspecific activation with the cytokines IL-12, IL-15, and IL-18 or in response to antigens or cy

117 The interleukin (IL)-12-type cytokines IL-12 and IL-23 are involved in T-helper (Th) 1 and Th17

118 cted the presence of two dominant cytokines (IL-12 and IL-6) clustering with CD68(+) monocyte/macroph

119 uction of key proinflammatory Th1-cytokines (IL-12, TNF-alpha, IFN-gamma, IL-6, and IL-8), and prefer

120 crease during NK stimulation with cytokines (IL-12, IL-18, and IL-15).

121 ignature TH1- and TH17-polarizing cytokines, IL-12 and IL-23, respectively.

122 T cell polarization resulted from decreased IL-12 secretion by Treg-DC, which may be post-transcript

123 conventional pathway of NK-cell development, IL-12-driven CD122(+)CD49b(+) cells remain confined to a

124 way regulated by CB1, able to promote either IL-12 and IL-23 release from keratinocytes or TH1 and TH

125 tenin-stabilized CD8a+ DCs secreted elevated IL-12 upon in vitro microbial stimulation, and pharmacol

126 chanism for regulation of the genes encoding IL-12 (Il12a and Il12b; collectively called 'Il12' here)

127 ng stimulation with exogenous and endogenous IL-12.

128 sgenic IL-12 was short-lived, but endogenous IL-12 expression was induced, and both IL-12 and IFN-gam

129 refore links the STING-IRF3 axis to enhanced IL-12 production and intracellular bacterial control in

130 timulate secretion of tumor necrosis factor, IL-12, and IL-6 and CD4 T-cell activation.

131 locyte macrophage-colony stimulating factor, IL-12, -13, and -15, which was prevented with ex vivo tr

132 enesis of the founding member of the family, IL-12.

133 cell differentiation, a reduced capacity for IL-12 production, but increased IL-10 production compare

134 de bridges in IL-12alpha are dispensable for IL-12 secretion, stability, and biological activity.

135 y chronic infection and provide evidence for IL-12 as a key factor driving these responses.

136 ciation of Jak2 with IL-23R is mandatory for IL-12 and/or IL-23 signaling, whereas Tyk2 seems to be d

137 ated macrophages constitutively positive for IL-12/23 p40 and capable of activating neonatal LTi cell

138 xes, with IL-12Rbeta2 as second receptor for IL-12 and IL-23R for IL-23 signal transduction.

139 These findings reveal a critical role for IL-12 in shaping the anti-inflammatory biofilm milieu by

140 More important, exosomes from IL-12-stimulated CTLs directly activated bystander naive

141 ys the basis for a simplified yet functional IL-12 cytokine.

142 Furthermore, IL-12-mediated protection required NADPH oxidase activit

143 ein levels of Th1-type cytokines (IFN-gamma, IL-12) and Th2-type cytokines (IL-6, IL-10) were signifi

144 The serum levels of IFN-gamma, IL-12, IL-6, and granulocyte colony-stimulating factor w

145 mechanism could then initiate the IFN-gamma/IL-12 feedback circuit, a key amplifier of DC lymph node

146 uction of antibody to P. gingivalis, greater IL-12 expression, and more plasma cells in lymph nodes f

147 cretion of biologically active heterodimeric IL-12.

148 L-12p35 subunit is shared by 2 heterodimers: IL-12 and IL-35.

149 iferative and effector responses were highly IL-12-dependent in blocking studies.

150 Heparin and HS were found to bind human IL-12 (hIL-12) with low micromolar affinity and increase

151 cells were incubated with recombinant human IL-12 (p70) in a dose- (0 to 10 ng/mL) and time-dependen

152 RV-infected mice showed further increases in IL-12 and increased expression of IFN-gamma, TNF-alpha,

153 cate that assembly-induced folding is key in IL-12 family biogenesis and secretion.

154 s toward a proinflammatory phenotype include IL-12 for TH1-like and IL-6 for TH17-type Tregs.

155 ion of pro-inflammatory cytokines including, IL-12, IFN-gamma, TNF-alpha, IL-2, IL-6 and IL-17 in the

156 the NF-kappaB pathway, inducing an increased IL-12 production.

157 ll differentiation was hampered by increased IL-12 and IL-6 production.

158 y impacts type 2 responses through increased IL-12/23p40 production.

159 -infected mice was associated with increased IL-12-producing CD103(+) lung DCs.

160 Induced IL-12 expression in hyperoxia-exposed, RV-infected mice

161 DED-induced IL-12 and IL-23 are required for in vivo transition of p

162 ine family as consisting of pro-inflammatory IL-12 and IL-23 and the anti-inflammatory IL-27 and IL-3

163 peritoneal macrophages, which can influence IL-12 production.

164 the mechanism(s) by which heparin influences IL-12 bioactivity.

165 Additionally, eATP inhibited IL-12 production whereas IL-10 levels remained unchanged

166 versal of helminth suppression of the innate IL-12 response of CD8alpha(+) dendritic cells, which occ

167 of Acanthamoeba produced significantly less IL-12 and IL-6 than the Neff strain.

168 Hyperoxia increased lung IL-12 expression, which persisted up to 12 d postexposur

169 ow levels of HLA-I with activated NKp30/MAPK/IL-12 (interleukin-12) or IL-2 (interleukin-2) pathway w

170 Also, AD inflammatory mediators (e.g. MMP12, IL-12/IL-23p40, CXCL9, CCL22, PI3/Elafin) correlated bet

171 In animal models, IL-12 and IL-23 participate in the development of malign

172 e ZXDC gene, biologically linked to monocyte IL-12 production through CCL2/MCP1.

173 eno-associated viral vectors encoding murine IL-12 or luciferase under the control of a liver-specifi

174 oHSV G47Delta expressing murine IL-12 (G47Delta-mIL12), antibodies to immune checkpoints

175 Within the native IL-12 heterodimer, composed of IL-12alpha and IL-12beta,

176 one marrow T cell activation is nonspecific, IL-12-dependent, and induces innate memory T cell phenot

177 L-27, and aldehyde dehydrogenase 1A2 but not IL-12 or IL-35; IL-10 and TGF-beta together drove their

178 Notably, IL-12 converted human ILC2 cells into ILC1 cells, and th

179 ovirus (Ad-TD) to deliver non-secreting (ns) IL-12 to tumor cells and examine the therapeutic and tox

180 However, the adjuvant activity of IL-12 is short-lived due to regulatory T cell (Treg) rei

181 induced secretion and biological activity of IL-12 versus misfolding and degradation of IL-12alpha.

182 rin in modulating the biological activity of IL-12.

183 rolonged exposure to IL-2, or by addition of IL-12 to cultures, revealing that cytokine signaling cou

184 bearing mice with systemic administration of IL-12 in combination with intratumor injection of anti-H

185 y associated with systemic administration of IL-12 precludes its clinical application.

186 restingly, p40 was involved in the arrest of IL-12 receptor (IL-12R) IL-12Rbeta1, but not IL-12Rbeta2

187 mportant questions about how the assembly of IL-12 family members is regulated and controlled in the

188 protein production was due to attenuation of IL-12 mRNA association with polyribosomes inhibiting tra

189 We show that transient blockade of IL-12 and IFN-gamma during priming promotes the developm

190 ndings offer renewed hope for development of IL-12-based treatments for cancer.

191 The disruption of IL-12 promotes angiogenesis and increases blood flow rec

192 To determine the effect of IL-12, hPDL cells were incubated with recombinant human

193 We investigated the effects of IL-12 inhibition on vascular and left ventricular (LV) f

194 STAT4 deficiency as a novel inborn error of IL-12-dependent IFN-gamma immunity associated with susce

195 a circuit that fine-tunes the expression of IL-12 by iNOS in macrophages, potentially enabling versa

196 This study underlines the importance of IL-12 p40 monomer (p40) in helping cancer cells to escap

197 Under the influence of IL-12, hPDL cells expressed significantly higher levels

198 ng intensity is low; or in the inhibition of IL-12 synthesis and maintenance of intestinal mucosal ho

199 a significantly greater expression level of IL-12, GM-CSF, and interferon-gamma (IFN-gamma) than eit

200 production in response to elevated levels of IL-12 and IL-18.

201 e in NK cell activation, augmented levels of IL-12, IL-15, IL-18, IFN-gamma, and TNF were detected in

202 Conditioned medium of IL-12-incubated cells proved to contain molecule(s) that

203 animals are rescued by the neutralization of IL-12 or IFNgamma.

204 O(+) DC in the tumor-draining lymph nodes of IL-12 plus GM-CSF-treated tumor-bearing mice revealed th

205 Underlying signaling pathways of IL-12 were determined by using specific inhibitors.

206 Deletion of the N-terminal signal peptide of IL-12 can effect such a change by preventing IL-12 secre

207 e polyclonally stimulated in the presence of IL-12 and IL-21 to generate TFH cells.

208 BA led to a markedly increased production of IL-12 and IFN-gamma, but not of TNF-alpha, IL-6, and IL-

209 g in DCs, leading to increased production of IL-12 and increased differentiation of T lymphocytes tow

210 is kinase is important for the production of IL-12 and TNF-alpha by macrophages and dendritic cells e

211 trol the otherwise deleterious production of IL-12 by CD103(+) CD11b(-) DC.

212 signaling was shown to inhibit production of IL-12 by CD40L-activated DCs.

213 Mechanistically, steady-state production of IL-12 by migratory CD103(+) DCs, independent of signals

214 6 and CD40 expression, and the production of IL-12 p70, IL-2, IL-6, and TNF-alpha by beta-glucan-stim

215 Interestingly, LPS-induced production of IL-12 was STAT2 and type I IFN receptor (IFNAR) dependen

216 nt of DCs, leading to enhanced production of IL-12, which is essential for PG545-mediated NK cell act

217 ted lung injury, and increased production of IL-12/23p40, which, when neutralized, restored IL-13 pro

218 ersus 4%), as well as a greater reduction of IL-12 (-25% versus -4% versus -2%), malondialdehyde (-27

219 phosphorylation and consequent reduction of IL-12 synthesis.

220 l systems and suggests an osteolytic role of IL-12 in pathogenesis of periodontal disease.

221 Yet, a possible role of IL-12 in periodontal disease has not been clarified.

222 e observed a markedly increased secretion of IL-12 and TNF-alpha by CXCL4-moDCs exclusively upon stim

223 ytosis and decreased macrophage secretion of IL-12 p40.

224 T cell capable of constitutive secretion of IL-12, and delineate the mechanisms via which these CAR

225 ranscriptional control on the p35 subunit of IL-12.

226 Suppression of IL-12 protein production was due to attenuation of IL-12

227 erculosis induction of IL-10, suppression of IL-12, and inhibition of class II major histocompatibili

228 demonstrate helminth-induced suppression of IL-12-dependent differentiation of killer-like receptor

229 demonstrate helminth-induced suppression of IL-12-dependent differentiation of killer-like receptor

230 cells upon BCG stimulation was dependent on IL-12 and IL-18.

231 ulated in men exposed to combat traumas, one IL-12-mediated signaling module upregulated in men expos

232 hosphorylation in response to either IL-2 or IL-12/15 cytokine combinations.

233 ulated with an anti-CD3 antibody and IL-4 or IL-12, with and without the presence of NSAIDs.

234 ls synergistically with TCR signaling and/or IL-12.

235 e pancreatitis induced by either cerulein or IL-12 + IL-18.

236 other cytokines, respectively, IFN-gamma or IL-12 if activated by IL-2, or IL-5 if activated by IL-4

237 nderlying the possible roles of IFN-gamma or IL-12 in M1-mediated inhibition of osteoclastogenesis.

238 s expressed by human NK cells after NKG2D or IL-12 plus IL-18 stimulation and by mouse NK cells durin

239 n cytokines known to affect disease outcome: IL-12, type I IFN, and IL-27.

240 ter levels of p40 than p40 homodimer (p402), IL-12, or IL-23.

241 r basis of persistent IDO expression in post-IL-12 DC.

242 e cellular and molecular biology of the post-IL-12 regulatory rebound and provide insight into how fe

243 Four weeks postinfection, IL-12, type 1 IFN, and IL-27 were all required for effic

244 IL-12 can effect such a change by preventing IL-12 secretion from cells.

245 he ability to sense inflammation and produce IL-12, leading to improved primary CD8 T cell responses

246 m peripheral blood of healthy donors produce IL-12 and other proinflammatory cytokines when exposed t

247 dAIH secrete high levels of proinflammatory IL-12 and IL-6, suggesting that this inflammatory milieu

248 Thus, glucose promoted IL-12-independent Th1 differentiation, whereas aromatic

249 In psoriasis, IL-12/23 inhibition results in a greater improvement of

250 Recently, IL-12 emerged as a critical player in type 2 diabetes co

251 In addition, HOCl significantly reduced IL-12 production in mBMDC.

252 in addition to processing RA, also secreted IL-12 and were responsible for gut imprinting specificit

253 Despite sharing the IL-12p35 subunit, IL-12 (IL-12p35/IL-12p40) promotes inflammatory response

254 d apoptotic cell-driven IL-10 and suppressed IL-12 production in a GCN2-dependent mechanism.

255 Activation of C5aR2 in NK cells suppressed IL-12/IL-18-induced IFN-gamma production.

256 l responses to infected B cells by targeting IL-12, MHC class II, and lysosomal proteases.

257 10), Th1 (CXCL10, CXCL11) and Th1/Th17/Th22 (IL-12/IL-23p40) responses.

258 Previous studies demonstrated that IL-12-driven antitumor activity is short-circuited by a

259 Proteomic analysis demonstrates that IL-12 stimulation alters catalytic and binding activitie

260 Cell fractionation studies determined that IL-12 and TNF-alpha secretion is limited to CD16(+) mono

261 In this study, we determined that IL-12 disruption rescued angiogenesis and arteriogenesis

262 erculosis Ag TB10.4 (EsxH), we observed that IL-12 is the dominant cytokine driving both CD8(+) T cel

263 thogenesis based on the documented role that IL-12 and IL-23 play in autoimmune diseases through diff

264 In this study, we show that IL-12 and other proinflammatory cytokines transduce sign

265 We show that IL-12 production by colonic CD103(+) CD11b(-) DC is repr

266 sting of the IL-23 receptor (IL-23R) and the IL-12 receptor beta1 (IL-12Rbeta1).

267 Recent studies have identified the IL-12 cytokine family as consisting of pro-inflammatory

268 adaptive immune maturation by modulating the IL-12/IL-12R pathway and the novelty of the OT-II.Ncf1(m

269 Interleukin (IL)-27, a member of the IL-12 cytokine family, plays an important and diverse ro

270 Members of the IL-12 family perform essential functions in immunoregula

271 erleukin 35 (IL-35) is a novel member of the IL-12 family, consisting of an EBV-induced gene 3 (EBI3)

272 ntrol granzyme B through upregulation of the IL-12 receptor.

273 ism and pSS and elucidate involvement of the IL-12/IL-35 balance in patients with pSS by using functi

274 Our findings emphasize involvement of the IL-12/IL-35 balance in the pathogenesis of pSS.

275 -resident ILC1s in a manner dependent on the IL-12 receptor and STAT4.

276 They share the IL-12 receptor beta1 (IL-12Rbeta1) as one component of t

277 hanism for ILC2 plasticity was mapped to the IL-12-IL-12R signaling pathway and was confirmed through

278 aveolin and caused cancer cell death via the IL-12-IFN-gamma pathway.

279 Thus, IL-12 is a major signal promoting priming in the lymph n

280 d leukotriene B4, and ELISAs quantified TNF, IL-12 and IL-10 in the gingival tissues.

281 n part, to be the consequence of exposure to IL-12.

282 nd T-bet and enhanced capacity to respond to IL-12 and IL-18 stimulation.

283 cells into an ILC1 phenotype in response to IL-12.

284 ed an increased functional responsiveness to IL-12 and IL-18, as well as to K562 cells, indicating th

285 Interestingly, transgenic IL-12 was short-lived, but endogenous IL-12 expression w

286 , low and transient expression of transgenic IL-12 in hepatocytes causes loss of tolerance to hepatoc

287 e treatment with Ad-TD expressing unmodified IL-12.

288 Adeno-associated virus IL-12-treated mice developed histological, biochemical,

289 ssential for melanocyte homeostasis, whereas IL-12 supported nevus development.

290 ter regulator of osteoclastogenesis, whereas IL-12 increased the apoptosis of osteoclasts, suggesting

291 aim of this study is to investigate whether IL-12 affects expression of receptor activator of nuclea

292 entation and a novel mechanism through which IL-12 and IL-7 synergistically control granzyme B throug

293 We report that upon activation with IL-12, IL-15, and IL-18 human NK cells express NKG2D lig

294 te effector CD8 T cells, in combination with IL-12, or more surprisingly IL-2, it induced striking an

295 erestingly, further stimulation of CTLs with IL-12 impacts exosome size and leads to selective enrich

296 IL-36 exerts a synergic adjuvant effect with IL-12, enhancing Th1 polarization in adult (AD) mice, we

297 Stimulation with IL-12 and IL-23 results in activation of receptor-associ

298 ys and, in particular, by supplementing with IL-12.

299 ndent but dependent on IL-18 in synergy with IL-12, IL-15 and/or interferon-alpha/beta.

300 rior studies demonstrating that therapy with IL-12 (the cytokine encoded in part by IL12B, associated