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1 IL-12 p40 expression occurred only in monocytes/macropha
2 IL-12 p40 mRNA and IL-12 p70 protein were also found to
3 IL-12 p40 mRNA was up-regulated in a dose-dependent mann
4 IL-12 p40 subunit mRNA by using the patient's PBMCs afte
5 IL-12 p40, IFN-gamma, TNF, IL-1alpha, and IL-6 were show
6 IL-12 p40-deficient mice (12KO) were resistant to EAU in
7 , interleukin-1beta (IL-1beta), IL-6, IL-10, IL-12 p40, alpha interferon (IFN-alpha), and IFN-gamma,
8 gingivalis LPS-induced production of IL-10, IL-12 p40, and IL-12 p70 by human monocytes was investig
11 ntracellular cytokine staining (IL-5, IL-10, IL-12 p40, TNF-alpha, and IFN-gamma) and cytometric bead
12 ioimmunoassays, interleukin-4 (IL-4), IL-10, IL-12 p40, tumor necrosis factor alpha (TNF alpha), inte
13 serum, significant decreases in IL-6, IL-10, IL-12 p40, tumor necrosis factor-alpha, IFN-gamma, and I
15 cytes that expressed the Th1 cytokines IL-2, IL-12 p40, and IFN-gamma mRNA was markedly diminished in
16 Expression of cytokines IL-2, IL-4, IL-5, IL-12 p40, IL-13, and interferon gamma is not affected b
17 crease expression of IL-1beta, IL-1Ra, IL-8, IL-12 p40, RANTES, macrophage inflammatory protein-1alph
19 ependent role for EKLF binding in activating IL-12 p40 transcription in resting RAW264.7 cells, where
22 by reverse transcription-PCR amplification, IL-12 p40 mRNA was constitutively expressed in LC RNA ex
23 is comprised of an IL-12 p35 subunit and an IL-12 p40-related protein subunit, EBV-induced gene 3 (E
25 owever, reduced expression of both IL-10 and IL-12 p40 mRNA were found in Mac-3+ cells from male mice
26 e eliminated the reduction of both IL-10 and IL-12 p40 mRNA, suggesting that the Th2 inducer phenotyp
27 n, because mice deficient for both IL-10 and IL-12 p40 show no intestinal pathology following H. hepa
28 ated with high growth of Mtb, high IL-10 and IL-12 p40, nearly undetectable IL-12 p70 levels, and the
30 inducible nitric-oxide synthase, IP-10, and IL-12 p40 mRNA, whereas no increase or relatively small
32 arriers had higher serum levels of IL-12 and IL-12 p40 in comparison with controls (P < 0.01), sugges
34 ors, including TNF, CCL5, CXCL10, IL-18, and IL-12 p40, and identified 140 drugs targeting 16 of them
35 induction of I-A, CD80, CD86, IL-1beta, and IL-12 p40 while inhibiting the expression of IL-10, sugg
38 ntial effects on production of TNF-alpha and IL-12 p40 by human monocytes, whereas MPL-induced activa
40 stimulated spleen reduced both TNF-alpha and IL-12 p40 production, but 33D1+ dendritic cell removal o
43 on, including the expression of CD8alpha and IL-12 p40 as well as major histocompatability complex cl
44 comparable expansions of dendritic cells and IL-12 p40 productive capacity in both infected and uninf
45 iderably greater expression of IFN-gamma and IL-12 p40 mRNAs in the LN draining a locally controlled
47 s in response to IRBP: reduced IFN-gamma and IL-12 p40, but unchanged levels of TNF-alpha, IL-4, IL-5
48 ponses in anti-CD40-treated IFN-gamma-/- and IL-12 p40-/- C57BL/6 mice were unaffected, although anti
49 ospot assays indicated that IFN-gamma-/- and IL-12 p40-/- gene knockout mice developed CTL responses
53 Mitigated induction of COX-2, IL-12 p35, and IL-12 p40 gene expression by CD11b/CD18-deficient macrop
54 r optimal induction of COX-2, IL-12 p35, and IL-12 p40 genes by low concentrations of LPS or by all c
58 ndeed, neutralizing endogenous p40 with anti-IL-12 p40 mAb reduced Th1 development in p35-/- allograf
59 of infected colitic IL-10 KO mice with anti-IL-12 p40 resulted in markedly reduced intestinal inflam
61 nal, since inhibition of this pathway blocks IL-12 p40 promoter activity in macrophage cell lines and
64 ng with IFN-gamma, through increases in both IL-12 p40 and p35 mRNA levels, caused a significant incr
65 he mechanism(s) of IL-10 suppression of both IL-12 p40 and IL-12 p35 genes is primarily seen at the t
67 udies, we observed increased amounts of both IL-12 p40 monomer and homodimer in the serum of C57BL/6
68 iple apoptotic pathways, dependent upon both IL-12 p40 and FasL, that may play a role in the lethal p
69 nally, injection of the pIL-12o- into BALB/c IL-12 p40-/- mice also resulted in a biphasic pattern of
70 (IFN-gamma 0/0) produced as much circulating IL-12 p40 and IL-12 p70 as did IFN-gamma +/+ mice follow
75 scription factor in macrophages, controlling IL-12 p40 production induced by bacterial products and t
76 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-
77 e 1, resulted in production of the cytokines IL-12 p40 and TNF-alpha by a mechanism independent of re
78 the set of p38 MAPK-dependent genes in DCs (IL-12 p40 and cellular inhibitor of apoptosis protein-2)
79 suggest a novel role for epithelial-derived IL-12 p40 in modifying the level of airway inflammation
81 minant-negative construct of PU.1 diminishes IL-12 p40 promoter activity and endogenous IL-12 p40 pro
84 responded to RANKL stimulation with elevated IL-12 p40 mRNA expression, Peyer's patch DC instead pref
88 y transfectable and regulates the endogenous IL-12 p40 gene in response to IFN-gamma or LPS similarly
89 molecular events occurring at the endogenous IL-12 p40 locus in lipopolysaccharide-stimulated periton
91 ed LC maturing into dendritic cells, express IL-12 p40 mRNA, as well as p40 and functional p70 protei
92 -specific CD4+ T cells transduced to express IL-12 p40 into mice immunized to develop experimental au
94 a 0/0 mice generated two- to threefold fewer IL-12 p40-secreting cells following in vitro or in vivo
95 c protein-immunopositive cells colabeled for IL-12 p40 RNA; indicating that LPS-stimulated astrocytes
96 tory effect at the transcriptional level for IL-12 p40 without down-regulation of the IL-12 p35 gene.
100 ally resistant, animals lacking a functional IL-12 p40 gene were found to be highly susceptible to M.
102 n of (pro)inflammatory cytokines (IFN-gamma, IL-12 p40, and TNF-alpha) and NO in response to myelin b
107 w evidence that full activation of the human IL-12 p40 promoter may result primarily from the interpl
108 ll line RPMI-8866, we localized to the human IL-12 p40 promoter two essential cis elements, the NFkap
109 he CACCC element (-224 to -220) on the human IL-12 p40 promoter was observed in resting human primary
113 s after WNV infection, and mice deficient in IL-12 p40 and IL-23 p40 (Il12b(-/-)) or IL-23 p19 (Il23a
116 organisms had induced a 27-fold increase in IL-12 p40 mRNA levels while killed organisms had induced
118 ere accompanied by substantial reductions in IL-12 p40 and IL-12 p70 protein in both IRF-1(-/-) and I
120 ments are found to have an important role in IL-12 p40 promoter activation by lipopolysaccharide.
121 pression of inflammatory cytokines including IL-12 p40, and depletion of IL-12 p40 from p50(-/-)p65(+
122 d proinflammatory gene expression, including IL-12 p40, TNF-alpha, and inducible nitric oxide synthas
125 eficient mice demonstrate markedly increased IL-12 p40 protein and mRNA expression compared with wild
126 tment in these conditions revealed increased IL-12 p40 homodimer (p80) levels were associated with en
128 ination of endogenous IL-10 led to increased IL-12 p40 production in DCs as well as increased prolife
129 0 in a strain-specific manner, and increases IL-12 p40, IFN-gamma-inducible protein-10, and IFN-gamma
130 ysaccharide (LPS) from B. abortus can induce IL-12 p40 mRNA expression and protein secretion by human
131 stablished from ICSBP-/- mice did not induce IL-12 p40 transcripts, nor stimulated IL-12 p40 promoter
136 gest that inhibition of H. hepaticus-induced IL-12 p40 expression by NF-kappaB subunits is critical t
137 on (IFN)-gamma on lipopolysaccharide-induced IL-12 p40 in murine macrophages and alters IFN-gamma sig
138 P) inhibits lipopolysaccharide (LPS)-induced IL-12 p40 mRNA expression, protein production, and promo
139 ability of IFN-gamma to augment LPS-induced IL-12 p40 mRNA further when both stimuli were present si
144 IFN-beta-1b significantly inhibits inducible IL-12 p40 up to 80% and biologically active IL-12 p70 up
148 ce express lower levels of gamma interferon, IL-12 p40, and inducible nitric oxide synthetase 2 (NOS2
150 response to LPS, IRF.1-/- mice produced less IL-12 p40, IL-12 p35, and IFN-gamma mRNA in the liver th
152 o a marked induction of both human and mouse IL-12 p40 promoter activities in ICSBP+/+ and ICSBP-/- c
153 trast, anti-huIL-12Rbeta1 mAb 2B10 and mouse IL-12 p40 subunit homodimer (mo(p40)2) blocked 125I-huIL
155 Mutations from -79 to -74 in the murine IL-12 p40 promoter significantly reduce lipopolysacchari
156 defective adenoviruses containing the murine IL-12 p40 subunit (Ad.mp40) or a bicistronic vector cont
157 0 days before infection increased lymph node IL-12 p40 productive capacity 20-fold compared to that o
159 ility was further supported when we observed IL-12 p40 overexpression selectively in airway epithelia
160 osis during infection, but in the absence of IL-12 p40 and functional FasL, activation of this transc
161 us or LPS also inhibited the accumulation of IL-12 p40 mRNA, but did not inhibit IL-12 p35 and TNF-al
162 ively inhibits transcriptional activation of IL-12 p40 and p35 genes while potently activating IL-10
163 ced signaling pathways for the activation of IL-12 p40 gene expression, or an abnormality in the IL-1
170 f IL-12 and TNF-alpha by splenocytes, and of IL-12 p40 by purified spleen CD8alpha(+) lymphoid dendri
173 results indicate that the local delivery of IL-12 p40 by T cells inhibited CIA by suppressing autoim
174 okines including IL-12 p40, and depletion of IL-12 p40 from p50(-/-)p65(+/-) mice ameliorates H. hepa
177 y acidic protein-p40 mice with expression of IL-12 p40 alone remained asymptomatic, with no inflammat
178 eover, MFAg inhibited the mRNA expression of IL-12 p40 and IL-10 as assessed by RNA protection assays
179 lective impairment in the mRNA expression of IL-12 p40 but not IL-1alpha, IL-1beta, IL-1Ra, IL-6, IL-
184 f IL-10 to control LPS-induced expression of IL-12 p40 was significantly compromised in macrophages l
185 This study underlines the importance of IL-12 p40 monomer (p40) in helping cancer cells to escap
191 MIP-3beta correlated with the inhibition of IL-12 p40 and TNF-alpha production by monocytes and with
193 un-on assays revealed that the inhibition of IL-12 p40, IL-12 p35, and TNF-alpha was at the gene tran
198 des expressed up to 10-fold higher levels of IL-12 p40 and inducible (type 2) nitric oxide synthase m
200 olitis is associated with elevated levels of IL-12 p40 expression, and p50/p105-deficient macrophages
201 hepaticus induced markedly higher levels of IL-12 p40 in p50(-/-)p65(+/-) macrophages than in WT mac
202 ficient macrophages express higher levels of IL-12 p40 than wild-type macrophages after challenge wit
205 ntified as astrocytes, while the majority of IL-12 p40 RNA-expressing cells appeared to be microglia.
206 lts placed epithelial cell overgeneration of IL-12 p40 as a key intermediate for virus-inducible infl
207 ve mice were also examined for production of IL-12 p40 mRNA following exposure to the viable or kille
209 entified to be involved in the regulation of IL-12 p40 gene expression by LPS and IFN-gamma, i.e., c-
210 e was induced by EKLF for down-regulation of IL-12 p40 transcription in activated RAW264.7 cells, but
215 play a pivotal role in the superinduction of IL-12 p40 observed after challenge of macrophages lackin
216 ast, iC3b binding resulted in suppression of IL-12 p40 mRNA and significantly inhibited the productio
217 e hypothesize that the impaired synthesis of IL-12 p40 in ICSBP-/- animals is the primary lesion resp
220 ponses in vivo, primarily through the use of IL-12 p40 gene-targeted mice and neutralizing antibodies
223 Nevertheless, in contrast to IFN-gamma-/- or IL-12 p40-/- animals, iNOS-deficient mice survived acute
225 e mice deficient in IFN-gamma, IL-12 p35, or IL-12 p40 all succumbed to LVS doses that were sublethal
227 LPS was a more potent inducer of IL-12 p35, IL-12 p40, and IFN-gamma mRNA, as well as of IL-12 prote
228 ased the induction of MPL-induced IL-12 p35, IL-12 p40, and IFN-gamma mRNA, suggesting that the enhan
229 to induce interleukin-10 (IL-10), IL-12 p35, IL-12 p40, gamma interferon (IFN-gamma), glucocorticoid
230 tion of cyclooxygenase 2 (COX-2), IL-12 p35, IL-12 p40, TNF-alpha, IFN-inducible protein (IP)-10, and
232 oluble CD40 ligand agonist failed to produce IL-12 p40 and IL-12 p70 protein; however, the deficient
233 phages for activation of the proinflammatory IL-12 p40 and anti-inflammatory IL-10 promoters, as well
234 e also mitigated in IRF-1-/- mice, pulmonary IL-12 p40 and IL-12 p35 mRNA were not dysregulated.
235 innate and acquired immunity, down-regulate IL-12 p40 and inducible NO synthase expression in LPS/IF
236 ption factor in macrophages able to regulate IL-12 p40 transcription depending on the cellular activa
237 ntly higher mRNA expression of the regulated IL-12 p40 subunit, but not IL-10, in sarcoid compared wi
238 ed with CpG but not control ODN up-regulated IL-12 p40 expression and release, and these effects were
239 gamma R ligation selectively down-regulates IL-12 p40 and p35 gene expression at the level of transc
240 actor which directly or indirectly regulates IL-12 p40 gene activation and, as a consequence, IFN-gam
241 resence or absence of this element repressed IL-12 p40 transcription in interferon gamma/lipopolysacc
242 Dual labeling in situ analysis revealed IL-12 p40 RNA-positive cells scattered throughout the br
243 efficiently phagocytose chlamydiae, secrete IL-12 p40, and present chlamydial antigen(s) to infectio
244 g TNF-alpha by as much as sixfold, but serum IL-12 p40 and IL-12 p70 responses increased by only twof
246 -23) is a heterodimeric cytokine that shares IL-12 p40 but contains a unique p19 subunit similar to I
248 induce IL-12 p40 transcripts, nor stimulated IL-12 p40 promoter activity after IFN-gamma/LPS stimulat
250 n addition, chloroquine treatment suppressed IL-12 p40 production in response to Legionella treatment
252 pha protein expression occurred earlier than IL-12 p40 protein but was not required for IL-12 inducti
255 s with multiple sclerosis (MS) suggests that IL-12 p40 may have a role in the pathogenesis of the dis
259 Jun and a mutant c-Jun molecule activate the IL-12 p40 promoter and synergistically activate the prom
260 tic cell lines synergistically activated the IL-12 p40 promoter, apparently overcoming the requiremen
262 ulation of nuclear binding activities at the IL-12 p40 NFkappaB half-site was induced by EKLF for dow
263 redominant Rel dimers capable of binding the IL-12 p40 Rel site were the p50/p65 and p50/c-Rel hetero
265 Polymorphisms within the genes encoding the IL-12 p40 subunit, IL12B, and one of the IL-23 receptor
269 tibody to IL-12 and in mice deficient in the IL-12 p40 gene, ischemia/reperfusion-induced increases i
270 ding to the unique p40 NF-kappaB site in the IL-12 p40 promoter, whereas binding patterns to Ets and
274 ptional level, and that the induction of the IL-12 p40 and p35 genes have different requirements for
275 accharide (LPS)-induced transcription of the IL-12 p40 gene, which encodes the heavy chain of the IL-
278 l transduction involved in activation of the IL-12 p40 promoter; the phosphorylation defects may be i
281 ad, an additional mechanism dependent on the IL-12 p40 protein, either alone or in another complex su
282 ith IL-12Rbeta1 primarily via regions on the IL-12 p40 subunit and with IL-12Rbeta2 via 20C2-reactive
283 the IL-12 subunits (p35 and p40) or only the IL-12 p40 subunit genes targeted to astrocytes in the mo
284 LPS-induced binding of NF-kappaB to the IL-12 p40 promoter NF-kappaB-binding site was not affect
285 subunit to the nucleus to transactivate the IL-12 p40 gene, ultimately resulting in decreased IL-12
287 ant cytokine was transiently administered to IL-12 p40-deficient mice during the first 2 wk of infect
289 e role of IL-12 in immunity to tuberculosis, IL-12 p40(-/-) mice were infected with M. tuberculosis a
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