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1 ntrol granzyme B through upregulation of the IL-12 receptor.
2 nd the interaction of these species with the IL-12 receptor.
3 eedback loop by competitively binding to the IL-12 receptor.
4 n and their competitive interaction with the IL-12 receptor.
5 n and LTalpha possibly through regulation of IL-12 receptor.
6 tat3/Stat4, indicating signaling through the IL-12 receptor.
7 t on Th development is the expression of the IL-12 receptor.
8 , THC injection suppressed the expression of IL-12 receptors.
9 the expression and activity of high affinity IL-12 receptors.
10  signal transduction downstream of IL-23 and IL-12 receptors.
11  T-cell proliferation, IFN-gamma production, IL-12 receptor accumulation, and the IL-12-promoted acqu
12                                The IL-23 and IL-12 receptors also share a subunit, IL-12Rbeta1, that
13 -resident ILC1s in a manner dependent on the IL-12 receptor and STAT4.
14 e conditions, BALB/c T cells fail to express IL-12 receptors and become unresponsive to IL-12, preclu
15 urred even though the level of expression of IL-12 receptors and IL-12-induced Janus kinase phosphory
16 ted by Ag, B10.D2 T cells express functional IL-12 receptors and maintain IL-12 responsiveness.
17  to the effects of IL-2 alone, expression of IL-12 receptors and STAT4 are unaffected or decreased by
18         Through expression of high levels of IL-12 receptors and STAT4, IL-2-primed NK cells show enh
19 by adding neutralizing anti-IL-12 Abs or the IL-12 receptor antagonist p40 homodimer to primary MLC.
20 ated with either anti-IL-12 Abs, or with the IL-12 receptor antagonist p40 homodimer.
21 imers of the p40 subunit of IL-12 are potent IL-12 receptor antagonists in some systems, we have repo
22 p40)2 and their competitive binding with the IL-12 receptor are essential for determining IL-12 bioac
23 0, respectively, which signal via the common IL-12 receptor B1 (IL-12RB1) and the cytokine-specific r
24 IFN-gamma were found to significantly modify IL-12 receptor beta 2 expression after T cell activation
25 ption factor T-box expressed in T cells, and IL-12 receptor beta 2 in CD4(+) T cells from the DLN and
26 ment was shown to suppress the expression of IL-12 receptor beta 2 mRNA, indicating that, in addition
27 lls, IFN-gamma-producing cells expressed the IL-12 receptor beta 2-chain after activation in the pres
28 kin 12 (IL-12) treatment in up-regulation of IL-12 receptor beta(2) mRNA during T(H)1 priming, and in
29  In this study, we ectopically expressed the IL-12 receptor-beta 2 (IL-12R beta 2) bicistronically wi
30                                          The IL-12 receptor-beta 2 (IL-12R beta 2) chain is expressed
31                                              IL-12 receptor beta1 (IL-12Rbeta1) and IL-12Rbeta2 are e
32                  Expression of IL-12 and the IL-12 receptor beta1 (IL-12Rbeta1) and IL-12Rbeta2 subun
33                               They share the IL-12 receptor beta1 (IL-12Rbeta1) as one component of t
34 a the IL-23 receptor (IL-23R) and the shared IL-12 receptor beta1 (IL-12Rbeta1) controls innate and a
35 consists of the unique IL-23R and the common IL-12 receptor beta1 (IL-12Rbeta1).
36 sting of the IL-23 receptor (IL-23R) and the IL-12 receptor beta1 (IL-12Rbeta1).
37  interleukin-12 (IL-12), their expression of IL-12 receptors beta1 and beta2 is increased, sensitizin
38  IL-10 production; in addition, they inhibit IL-12 receptor beta2 (IL-12Rbeta2) chain expression.
39 is driven by interleukin (IL)-12 through the IL-12 receptor beta2 (IL-12Rbeta2) chain, whereas differ
40 -12 was associated with a specific defect in IL-12 receptor beta2 (IL-12Rbeta2) mRNA expression by CD
41 nella, the level of mRNA expression encoding IL-12 receptor beta2 (IL-12Rbeta2) subunit was diminishe
42 is essential for the late-phase induction of IL-12 receptor beta2 (Il12rb2) and signal transducer and
43 nfected donors also failed to upregulate the IL-12 receptor beta2 chain (IL-12Rbeta2) in response to
44  This may be due to a down-regulation of the IL-12 receptor beta2 chain (IL-12Rbeta2) that accompanie
45 ive to IL-12 via increased expression of the IL-12 receptor beta2 chain and produced elevated levels
46 ferentiation- or lineage markers such as the IL-12 receptor beta2 chain and the chemokine receptor CC
47 on-gamma (IFN-gamma) alleles and by inducing IL-12 receptor beta2 expression.
48 , inducing STAT5-dependent expression of the IL-12 receptor beta2-chain (IL-12Rbeta2) and the transcr
49 12 programmed T(EM) through induction of the IL-12 receptor beta2.
50    Constitutive expression of high levels of IL-12 receptor by iNKT cells enabled instant IL-12-induc
51 tment also exhibited increased expression of IL-12 receptor chains, suggesting that IL-2 may enhance
52 oid tissues for months after MCMV infection, IL-12 receptor-deficient NK cells failed to expand and w
53 L)-12 treatment blocked Treg expansion in an IL-12 receptor-dependent fashion.
54  an important role for the regulation of the IL-12 receptor during the innate immune response after i
55 me (ACS), spontaneously express interleukin (IL)-12 receptors, even in the absence of antigenic stimu
56  the Fc portion of IgG (FcgammaRIII) and the IL-12 receptor expressed on NK cells.
57 xpressed high levels of CD18 and upregulated IL-12 receptor expression after IL-12 treatment in vivo.
58 sults in an early reduction of high affinity IL-12 receptor expression and activation.
59  demonstrates that Tpm1 exerts its effect on IL-12 receptor expression in a cell-autonomous manner, r
60                         Therefore, increased IL-12 receptor expression might be expected in the host
61 n 12 (IL-12) production from macrophages and IL-12 receptor expression on activated T cells.
62 .D2 and BALB/c mice show distinct control of IL-12 receptor expression.
63 zation of IL-12 in C3H mice blocks increased IL-12 receptor expression.
64         OVA-specific CD8 T cells lacking the IL-12 receptor fail to differentiate or mediate graft re
65 ess both the beta 1 and beta 2 chains of the IL-12 receptor (IL-12R) and tyrosine phosphorylate STAT4
66 y Th2 cells results from a selective loss of IL-12 receptor (IL-12R) beta 2 subunit expression.
67    NK cells costimulated via the FcR and the IL-12 receptor (IL-12R) exhibited enhanced levels of act
68 restingly, p40 was involved in the arrest of IL-12 receptor (IL-12R) IL-12Rbeta1, but not IL-12Rbeta2
69 Methods and Results- We examined the role of IL-12 receptor (IL-12R) signaling in the development of
70 the Fc portion of IgG (FcgammaRIIIa) and the IL-12 receptor (IL-12R), both constitutively expressed o
71                          Two subunits of the IL-12 receptor (IL-12R), IL-12R beta 1 and IL-12R beta 2
72 pment have included greater understanding of IL-12 receptors in Th1 development, data regarding IFN-g
73 e results demonstrate that regulation of the IL-12 receptor, independent of IL-4, is a point of contr
74              Costimulation of the T-cell and IL-12 receptors induced the transcription of CD28 in app
75 human NK cells via the IL-2 receptor and the IL-12 receptor induces significant IFN-gamma production,
76 n of naive T cells through their antigen and IL-12 receptors initiates differentiation programs that
77                  Expression of high affinity IL-12 receptors is required for IL-12-mediated IFN-gamma
78 of L. major-infected C3H mice upregulate the IL-12 receptor on CD4(+), CD8(+), and B220(+) cells.
79 ression of the beta1 and beta2 chains of the IL-12 receptor on T cells.
80                             The interleukin (IL)-12 receptor (R)beta2 subunit is the critical molecul
81 diate signals that emanate from the IL-4 and IL-12 receptors, respectively.
82 and activation of DCs, mediated by autocrine IL-12 receptor signaling in the Tvax.
83 iation in vivo is consistent with a block in IL-12 receptor signaling, because LSF blocked IL-12-driv
84 st to the direct recruitment of Stat4 by the IL-12 receptor, Stat4 activation by the human IFN-alpha
85 tion of patients and treatment with IL-1 and IL-12 receptor subunit beta 1 (Rb1) antibodies may also
86  cells revealed inadequate expression of the IL-12 receptor, thus establishing a link between CTL dif
87 tumours, we show that fusing a domain of the IL-12 receptor to IL-12 via a linker cleavable by tumour
88  IL-12-dependent expansion, independently of IL-12 receptor upregulation.