ライフサイエンスコーパス: IL-12

1 IL-12 and IL-23 blockade with anti-IL-12p40 treatment co

2 IL-12 is an immune-activating cytokine with such potenti

3 IL-12 signals via the IL-12Rbeta1.IL-12Rbeta2 receptor c

4 IL-12 was directly related to DeltaCES-D(total) among me

5 IL-12(+)CD38(+) iNOS(+) M (M1M ) located in the bacteria

6 IL-12) improved accuracy in detecting bona-fide memory C

7 IL-12-encapsulated complex coacervates significantly imp

8 IL-12/23p40 neutralization prevented MHC class II upregu

9 crosis factor alpha, interleukin-10 (IL-10), IL-12, IL-1alpha, IL-6, and IL-17.

10 , 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, CCL11,

11 nical cows had increased secretion of IL-10, IL-12, and IL-18 upon stimulation of peripheral blood mo

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

13 o measure TNF-alpha, IFN-gamma, IL-6, IL-10, IL-12, IL-17A, IL-17C and IL-22 using ELISA multiplex ki

14 flammatory cytokine, TNF-alpha, IL-6, IL-10, IL-12, IL-17A, IL-17C and IL-22 were observed in CRC pat

15 ytokines (TNF-alpha, IFN-gamma, IL-6, IL-10, IL-12, IL-17A, IL-17C and IL-22) in patients with colore

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

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

18 timulatory cytokine, such as interleukin 12 (IL-12) (rNDV-anti-CD28-murine IL-12 [mIL-12], rNDV-anti-

19 biological relevance is the interleukin 12 (IL-12) family.

20 ncoding SIVenv/SIVGag/rhesus interleukin 12 (IL-12) plus SIV(M766&CG7V) gD-gp120 proteins formulated

21 and that this is mediated by interleukin-12 (IL-12) activation of NK cells.

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

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

24 gnificantly higher levels of interleukin-12 (IL-12) and interferon gamma (IFN-gamma) by as early as 4

25 Interleukin-12 (IL-12) is a powerful cytokine that activates the innate

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

27 ntiate after activation with interleukin-12 (IL-12), IL-15, and IL-18, exhibit potent antitumor respo

28 adult CD11b(+) mDCs produced interleukin-12 (IL-12), which prevented Th2 cell development by promotin

29 nocyte-derived, mature, high-interleukin-12 (IL-12)-producing type 1 polarized dendritic cells (MDC1)

30 ile releasing cytokines (eg, interleukin-12 [IL-12], IL-23, IL-6, IL-27, IL-10, transforming growth f

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

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

33 ations of antigen-specific T-helper 1 (IL-2, IL-12, interferon-gamma) and T-helper 2 (IL-4, IL-5) cyt

34 f the p40 subunit shared by IL-12 and IL-23 (IL-12/23p40).

35 uction downstream of receptors for the IL-23/IL-12 pathways and type I interferon family, where it pa

36 ared with ustekinumab treatment (anti-IL-23/-IL-12).

37 CCL5, and CXCL9) or T cell modulatory (IL-4, IL-12, and IL-15) cytokines.

38 serum, including interleukin 2 (IL-2), IL-6, IL-12 (p70), tumor necrosis factor (TNF), and IL-10, was

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

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

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

42 ony stimulating factor (G.CSF), IL-13, IL-6, IL-12, interferon (IFN)-gamma, IFN-alpha, IL-2, IL-2 R,

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

44 mor necrosis factor alpha (TNF-alpha), IL-6, IL-12/23, IL-17, IL-4/13, IL-5, immunoglobulin E (IgE),

45 wer levels of IL-7R, responded less to IL-7, IL-12, or IL-23 cytokines, and were more prone to apopto

46 ry cytokines (Eotaxin, IL-1beta, IL-7, IL-8, IL-12/IL-23p40, IL-12p70, IL-13, IL-16, IP-10, MCP-1, MC

47 lated following activation, especially after IL-12 plus IL-18 stimulation.

48 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

49 gh the roles of cytokines such as TNF-alpha, IL-12, IFN-gamma, and IL-10 in immunity and pathogenesis

50 geting one of 7 mechanisms (IL-6, TNF-alpha, IL-12/23, CD20, COX2, BLgammaS, p38/MAPK14).

51 Although IL-12 alone is required for NK cell IFN-gamma production

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

53 ar mechanisms governing IL-27 biogenesis, an IL-12 family member that limits infections and autoimmun

54 ressing carcinogenesis was accompanied by an IL-12 to IL-23 shift with a consecutive development of a

55 ll types, including natural killer cells, an IL-12 indicator cell line, and primary peripheral blood

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

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

58 alteration by pLL of CD86, CD40, IL-10, and IL-12 responses to LPS in BMDC; however, we now show tha

59 K cell responses were dependent on IL-18 and IL-12, whereas IFN-gamma secretion was restricted by hig

60 L-5, IL-6 and IL-17 and antitumoral IL-2 and IL-12 in tumor-proximal lymph nodes, and increasing IL-2

61 lar determinant of balance between IL-23 and IL-12 expression, potentially governing immune responses

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

63 IL-23 and IL-12, two structurally related heterodimeric cytokines

64 ic model as well as efficacy in an IL-23 and IL-12-dependent mouse colitis model.

65 feration, and activation by IL-7, IL-23, and IL-12 by cell culture, flow cytometry, and phospho-flow

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

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

68 was associated with decreased cAMP, IL-6 and IL-12.

69 expression of IL-1beta, TNF-alpha, IL-6, and IL-12 at baseline and/or following Ag stimulation compar

70 olysis and production of IL-1beta, IL-6, and IL-12, and increasing bacterial burden.

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

72 IL-10 among AA and IL-12 among men were inversely related to Delta"positive

73 tumor necrosis factor alpha (TNF-alpha), and IL-12 levels were upregulated.

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

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

76 ate this response through direct contact and IL-12 secretion.

77 T cells showed enhanced CD40 expression and IL-12 secretion compared with DCs cocultured with CD4(+)

78 Sequential administration of FOLFOX and IL-12 gene therapy following stromal deactivation by RLN

79 (i) decreases in the levels of IFN-gamma and IL-12, (ii) an increase in the level of the inflammatory

80 matory cytokines, for example, IFN-gamma and IL-12, in CCR2i- versus vehicle-treated mice.

81 -associated variants modulate IFN-gamma- and IL-12-associated outcomes, and in turn, PRR-induced outc

82 demonstrated increased TLR4-, IFN-gamma- and IL-12-induced STAT1 and STAT4 phosphorylation and cytoki

83 orouracil, leucovorin, and oxaliplatin), and IL-12, successfully stimulates central memory T cells an

84 5 production, MSP-RON signaling pathway, and IL-12 signaling and production in macrophages, which are

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

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

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

88 calated anti-TNF therapy and eventually anti IL-12/23 neutralizing antibody (ustekinumab).

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

90 (SMD = 0.8, 95% CI [0.20-1.41]) and an anti-IL-12/23 antibody (SMD = 0.48, 95% CI [0.26-0.70]) had l

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

92 Effects of anti-IL-12/23 remained significant and anti-IL-6 antibodies b

93 mumab (anti-TNF-alpha) and ustekinumab (anti-IL-12/23).

94 eutrophil-depleted WT mice treated with anti-IL-12 mAb or neutrophil-depleted IL-12(-/-) mice.

95 ily of cytokines has four members, which are IL-12 (p40:p35), IL-23 (p40:p19), the p40 monomer (p40),

96 Interestingly, p40 arrested IL-12-, IL-23-, or p40(2)-mediated internalization of IL

97 sult was associated with decreased articular IL-12/23p40 and IFN-gamma levels.

98 to high-avidity, TCR-engineered T cells, as IL-12-primed, low-avidity T cells cause less autoimmune

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

100 s evoked by TLR2, 3, 4, 5, and 8, as well as IL-12 responses evoked by whole pathogens, were all redu

101 b modulated H3K4 and H3K27 trimethylation at IL-12, TNF-alpha, and arginase-1 promoters, respectively

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

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

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

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

106 a responses are characteristically driven by IL-12 secretion from myeloid cells.

107 n antigen-independent, innate-like recall by IL-12 and IL-18.

108 ased expression of the p40 subunit shared by IL-12 and IL-23 (IL-12/23p40).

109 CBD-IL-12 may potentiate CPI immunotherapy for immunological

110 collagen-binding domain fused to IL-12 (CBD-IL-12) in mice bearing aggressive mouse tumours, CBD-IL-

111 the administration of unmodified IL-12, CBD-IL-12 induced sustained intratumoural levels of interfer

112 Furthermore, CBD-IL-12 potently synergized with CPI to eradicate large es

113 n mice bearing aggressive mouse tumours, CBD-IL-12 accumulates in the tumour stroma due to exposed co

114 frequencies of CD45(+) IL-12(+) and CD11b(+) IL-12(+) cells in the uterus and spleen.

115 egnant mice had lower frequencies of CD45(+) IL-12(+) and CD11b(+) IL-12(+) cells in the uterus and s

116 In dendritic cells, IL-12 and CCL2 responses as evoked by TLR2, 3, 4, 5, and

117 gnancy-associated changes in innate cellular IL-12 responses on the adaptive immune response.

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

119 In contrast, IL-12 is considerably more inducible in GD-OF, cells fai

120 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-

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

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

123 ule (4-1BBL) and immunostimulatory cytokine (IL-12).

124 uced secretion of the Th1-inducing cytokine, IL-12, and increased release of proinflammatory cytokine

125 inumab, an antibody to p40, blocks cytokines IL-12 and IL-23, and is a highly effective and safe trea

126 n vitro was mediated by the innate cytokines IL-12 and IL-18 more than MR1-induced TCR signaling, sug

127 d not modulate the Th-1-polarizing cytokines IL-12 and IL-18.

128 he production of disease-resolving cytokines IL-12 and TNF-alpha.

129 nes such as the p40 subunit of the cytokines IL-12 and IL-13 (ustekinumab), IL-17 (secukinumab, ixeki

130 the biology of a group of related cytokines: IL-12, IL-23, and IL-27.

131 alyses indicate genistein and equol decrease IL-12/IL-18-induced IFN-gamma production by human NK cel

132 -gamma-induced gene expression and decreased IL-12-inducible upregulation of IFN-gamma.

133 rly inhibited IL-10 expression but decreased IL-12/23p40 expression, which is opposite to the effect

134 of signal transduction, genistein decreases IL-12/IL-18-induced total phosphorylated tyrosine, and p

135 heparin-based complex coacervate to deliver IL-12, in which heparin-binding motifs on IL-12 allow fo

136 700841 will directly suppress TYK2-dependent IL-12 and IL-23 signaling and Janus kinase 1-dependent s

137 d with anti-IL-12 mAb or neutrophil-depleted IL-12(-/-) mice.

138 s postinfection in the absence of detectable IL-12.

139 th psoriasis compared with ustekinumab (dual IL-12/IL-23 inhibitor), but comparative molecular effect

140 Blocking either IL-12 or IFNgamma in Tnfaip3(Lg-KO) mice restored Th2 re

141 CMV infection, when the TCR is not engaged, IL-12 signaling is essential, and TLR signaling is expen

142 Blocking IL-4 enhances IL-12 production by tumour-antigen-bearing mregDC1s, exp

143 ment to the peritoneal cavity, and exogenous IL-12 restored monocyte recruitment and protection of ca

144 of LPS-stimulated human skin DCs to express IL-12 and promote IFN-gamma secretion by CD4(+) T cells.

145 F) and T(h)1 differentiation and expression (IL-12, TNF-alpha, IFN-gamma) were enhanced in the neutro

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

147 r defect and uncovered a surprising role for IL-12 in initiation of disease.

148 tokine with a biological role different from IL-12, IL-23, and p40(2) in which it attenuates autoimmu

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

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

151 files (TNF- alpha receptor, IL-6, IFN-gamma, IL-12, IL-17, IL-22, and IL-23) of patients with achalas

152 On the other hand, IL-12, IL-23, and p40(2) did not exhibit such inhibitory

153 FN-gamma and to drive the maturation of high IL-12-producing DCs.

154 rulent strain induced less IL-10, but higher IL-12, in macrophages.

155 y induce IL-23 in human fibrocytes; however, IL-12 expression is essentially undetectable in these ce

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

157 Importantly, IL-12 preconditioning prevented exhaustion as LAG-3, PD-

158 This difference in IL-12/23p40 regulation correlated with the differential

159 lso observed decrease in p40 and increase in IL-12, IL-23, and p40(2) in serum of mice with experimen

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

161 of distinct LPS-induced genes that included IL-12, TNF-alpha, and IL-6 in primary bone marrow-derive

162 ction of cytokines and chemokines, including IL-12 and C-X-C motif chemokine 10.

163 ling of pro-inflammatory cytokines including IL-12, IL-23, and type 1 interferons.

164 n the early phase of inflammation, including IL-12, eotaxin, RANTES, IL-10 and interferon-gamma (p <

165 to regulate IL-12 family members, including IL-12 and IL-23.

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

167 sensitization of WT mice markedly increased IL-12-producing hapten-primed dendritic cell numbers in

168 migratory TNFRp55(-/-) DCs of MLN increased IL-12/23p40 compared with wild-type mice.

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

170 e marrow-derived macrophages and LPS-induced IL-12/18-IFN-gamma signaling in Artd1(DeltaMyel) mice.

171 and monocytes produce elevated inflammatory IL-12 and IL-23 in a GSK3alpha/beta-dependent manner upo

172 diated depletion of the microbiota inhibited IL-12/23p40 production by ileal macrophages.

173 Interestingly, IL-12 and anti-IL-10 Abs improved T cell proliferation i

174 inated response to superantigens and a later IL-12- and IL-18-dependent, IFNgamma-dominated response

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

176 Further, genistein limits IL-12/IL-18-mediated upregulation of IL-18Ralpha express

177 ceptor signaling drives an innate macrophage/IL-12/NK cell/IFN-gamma axis that prevents inappropriate

178 Consequently, this inhibits STAT1-mediated IL-12 induction in macrophages & STAT4-mediated IFN-gamm

179 on; in contrast, in IL-1beta-deficient mice, IL-12 secretion by CD11b(+) DCs prevails and supports an

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

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

182 his innate increased ability to produce more IL-12 and IFN-gamma provided early protection to the C5a

183 und 48 provided robust inhibition in a mouse IL-12-induced IFNgamma pharmacodynamic model as well as

184 Interestingly, although murine IL-12 also binds heparin, heparin did not enhance its ac

185 nterleukin 12 (IL-12) (rNDV-anti-CD28-murine IL-12 [mIL-12], rNDV-anti-PD1-mIL-12, and rNDV-anti-PDL1

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

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

188 imary T. gondii infection, in the absence of IL-12 using IL-12p35(-/-) mice or anti-IL-12p70, seconda

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

190 The addition of IL-12 during in vitro expansion boosts low-avidity T cel

191 Addition of IL-12 restored T-cell proliferation to baseline levels.

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

193 mmune system; however, the administration of IL-12 has been associated with immune-related adverse ev

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

195 plasma IFN-gamma following administration of IL-12/IL-18 versus control-fed animals (p < 0.0001).

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

197 IL-1beta and the sex-specific association of IL-12 with DeltaCES-D(total) were replicated for the "de

198 Importantly, binding of IL-12 and IL-23 to IL-12Rbeta1 is mediated by p40, and b

199 es significantly improved the bioactivity of IL-12 and provided protection from proteolytic cleavage

200 ue of Fcgamma receptor IIB; dual blockade of IL-12 and IL-23; and inhibition of Janus kinases.

201 These results show that blockade of IL-12 and/or IL-23 may transiently reduce AVI, with more

202 Importantly, blockade of IL-12, IL-23, or both significantly reduced control of p

203 ileum initiates lethal GVHD, and blockade of IL-12/23p40 may represent a readily translatable therape

204 Complementation of IL-12 and IL-23 was able to restore T cell differentiati

205 D significantly reduced the concentration of IL-12 and IL-17 in lymph nodes of treated and contralate

206 iated with increased serum concentrations of IL-12 and elevated CD40 expression on CD11c(+) dendritic

207 Low concentrations of IL-12 during T-cell priming biases immune responses towa

208 well established, the exact contributions of IL-12, IL-18, and TLRs remain unclear for these two acti

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

210 tb) was found to be due to downregulation of IL-12 and IL-22 cytokines.

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

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

213 and p38, without affecting the expression of IL-12 and IL-18 receptors.

214 -Rel was sufficient to restore expression of IL-12 and IL-1beta in caspase-8-deficient cells.

215 signaling to the TLR4-induced expression of IL-12 in different types of human myeloid APC.

216 t on monocytes by altering the expression of IL-12 induced by LPS, whereas only AmB induced IL-10 sec

217 Induction of IL-12 and IFN-gamma early during infection with L. monoc

218 stimulation, while ERK-mediated induction of IL-12/23p40 in DCs may promote priming of T helper 1 (Th

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

220 IFN-alpha-mediated inhibition of IL-12 production, rather than inhibitory receptor expres

221 monocyte-derived DCs leads to inhibition of IL-12 production.

222 On the other hand, inhibition of IL-12-IL-23, as compared with inhibition of TNF, has gre

223 Indeed, a single injection of IL-12 coacervate significantly inhibits the in-vivo grow

224 he severe- ME/CFS group had higher levels of IL-12 and lower levels of IL-13 than the recovered group

225 interleukin-6 (IL-6) and decreased levels of IL-12, IFN-gamma, and the JAK1, STAT1, NF-kappaB, and ex

226 mptoms, increased interleukin (IL) levels of IL-12, IL-17, IL-10, IL-5, CXCL9, E-Selectin and ST2/IL-

227 igher levels of DC-STAMP and lower levels of IL-12, relative to macrophages in tuberculoid leprosy le

228 p3(Lg-KO) mice harbored increased numbers of IL-12-expressing cDC1s and elevated PD-L1 expression in

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

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

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

232 trated ex vivo activation in the presence of IL-12-induced optimal CD8(+) T cell expansion and melano

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

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

235 pten-presenting dendritic cell production of IL-12 and the development of hapten-reactive CD4 T cells

236 te burden along with increased production of IL-12 and TNF-alpha.

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

238 phosphorylation and consequent reduction of IL-12 synthesis.

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

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

241 Ag+ monocytes are an essential source of IL-12 for both innate and adaptive IFNgamma production,

242 ERK-mediated suppression of IL-12/23p40 in macrophages may prevent excessive inflamm

243 e to the effect of ERK signaling blockade on IL-12/23p40 in macrophages.

244 xpansion of pre-mNK cells to be dependent on IL-12 and IL-18.

245 ary T. gondii infection that is dependent on IL-12 and IL-23.

246 adrenergic receptor), a process dependent on IL-12 and STAT4 signaling.

247 r show that the latter population depends on IL-12 produced by CD8alpha(+) type 1 dendritic cells (DC

248 er IL-12, in which heparin-binding motifs on IL-12 allow for its effective encapsulation.

249 d no significant effect on NO, TNF-alpha, or IL-12 production in response to LPS challenge, MEK2-defi

250 tion, which could be provided by IFN-beta or IL-12.

251 d- SCID or inducible NO synthase-, CD40-, or IL-12-deficient mice, indicating attenuation.

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

253 pendent on PRR-initiated autocrine/paracrine IL-12-induced STAT4 activation to generate IFN-gamma, wi

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

255 ty and promotes type I immunity by promoting IL-12/18 expression.

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

257 Furthermore, tumors in mice receiving IL-12 complex coacervate treatment displayed increased i

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

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

260 s cFos and IRF1, which are known to regulate IL-12 family members, including IL-12 and IL-23.

261 crophage and T cells, respectively, restored IL-12 and IFN-gamma cytokine levels and BMM -T cell inte

262 atment with an antagonistic peptide restores IL-12 and induces IL-10 expression by DCs treated with l

263 iled to upregulate T-bet and did not secrete IL-12 and Th2 cell responses normally developed in infan

264 Since IL-12 and IL-23 are related cytokines that share the com

265 Specifically, IL-12-dependent activation of STAT4, and unexpectedly ST

266 IL-13 suppressed IL-12 production by mouse skin-derived DCs in vitro and

267 molecule upregulation, and secretion of Th1 (IL-12)- and Th17 (IL-23, IL-1beta, and IL-6)-conditionin

268 Using these tools, we demonstrate that IL-12, IL-18, and TLRs are completely dispensable for th

269 In this study, we demonstrate that IL-12-primed T cells are resistant to PD-1/PD-L1-mediate

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

271 their regulatory requirements, we find that IL-12 signaling is necessary for the differentiation and

272 The IL-12 family of cytokines has four members, which are IL

273 In addition, an enrichment in the IL-12 family and type I interferon signaling pathways wa

274 atients indicates that neutralization of the IL-12 and IL-23 pathways does not ameliorate disease.

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

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

277 a better understanding of the biology of the IL-12 family provides new therapeutic opportunities.

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

279 The DNA hypermethylation of the IL-12/IFN-gamma pathway was associated with decreased IF

280 PCR) and observed that multiple genes of the IL-12/IFN-gamma signaling pathway (IL12B, IL12RB2, TYK2,

281 Interestingly, renewal of the IL-12/IL-10 milieu restores the ability of farnesol-diff

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

283 Interleukin (IL)-12 and IL-23 belong to the IL-12 type family and are composite cytokines, consistin

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

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

286 ration of a collagen-binding domain fused to IL-12 (CBD-IL-12) in mice bearing aggressive mouse tumou

287 -gamma production by NK cells in response to IL-12 and for an efficient immune defense against Lister

288 inally, our data demonstrate that this tonic IL-12 production requires TLR-MyD88 signaling independen

289 arison with the administration of unmodified IL-12, CBD-IL-12 induced sustained intratumoural levels

290 to produce IFN-gamma upon actR but not upon IL-12 stimulation.

291 mma released by Vdelta2(+) cells upregulates IL-12 secretion by DCs in a positive feedback loop.

292 hibiting adipose accumulation of ILC1s using IL-12 neutralizing antibodies attenuates adipose tissue

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

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

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

296 herapeutically beneficial if cocultured with IL-12 cytokine during in vitro expansion and highly effe

297 investigation of heparin's interactions with IL-12 family cytokines and for the use of heparin as an

298 ion of IFN-gamma by NK cells stimulated with IL-12 and IL-18, which is a crucial system for early IFN

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

300 chanistically, glucocorticoids together with IL-12, IL-15, and IL-18 not only upregulate PDCD1 transc