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1 CD154, as well as by lipopolysaccharide and interleukin 4.
2 n children who survived, and lower levels of interleukin 4.
3 x vivo with a combination of CD40 ligand and interleukin 4.
4 requires GITR, CD4(+) T cells, B cells, and interleukin-4.
5 M)-CSF-dependent manner but independently of interleukin-4.
6 type on CD8(+) T cells through production of interleukin-4.
7 cells by the quintessential type 2 cytokine, interleukin-4.
8 ced significant increases in serum levels of interleukin-4.
9 to release the immunomodulatory key cytokine interleukin-4.
10 tic cytokines interferon, interleukin-2, and interleukin-4.
11 oduced more gamma interferon (IFN-gamma) and interleukin-4.
14 phils, 2) serum IgE levels, 3) T2 cytokines (interleukin-4, -13, and -4 to interferon-gamma ratio), a
15 ess syndrome mortality, when increased, were interleukin-4 (18.0 [6.0-54.2]), interleukin-2 (11.8 [4.
16 h2) cells and innate lymphoid cells, such as interleukins 4, 5, and 13, as underlying the eosinophili
18 a sandwich immunoassay for the detection of interleukin-4, a cytokine that promotes proliferation an
19 )-adrenergic receptor (beta(2)AR) on a CD40L/interleukin-4-activated B lymphocyte increases the level
20 hich Arg1 expression is greatly increased by interleukin 4 and 13 signaling through the transcription
22 provoked concentrations of interleukin 3 and interleukin 4 and augmented levels of interleukin 12 in
23 NKT cells failed to secrete large amounts of interleukin 4 and interferon-gamma after activation; how
24 table safety, validating the crucial role of interleukin 4 and interleukin 13 in atopic dermatitis pa
25 ations have been seen in atopic asthma, with interleukin 4 and interleukin 13 thought to have a role
26 mation by potently inhibiting the binding of interleukin 4 and interleukin 13 to interleukin-4Ralpha
27 gE, a product of B cells from the actions of interleukin 4 and interleukin 13, is used as treatment f
28 ha monoclonal antibody) blocks signalling of interleukin 4 and interleukin 13, type 2/Th2 cytokines i
30 ers have established unanticipated roles for interleukin 4 and the alternative activation of tissue m
31 d produced TH2-inducing cytokines, including interleukin 4 and thymic stromal lymphopoietin, which ar
32 d produced TH2-inducing cytokines, including interleukin 4 and thymic stromal lymphopoietin, which ar
35 e immunized with a sopB mutant showed higher interleukin-4 and gamma interferon secretion levels than
36 as associated with increased serum levels of interleukin-4 and immunoglobulins G1 and E directed agai
37 and show substantively lower serum levels of interleukin-4 and interferon-gamma when compared with ma
41 TGF-beta signaling also led to a decrease in interleukin-4 and interleukin-13 concentrations, which d
42 receptor alpha monoclonal antibody, inhibits interleukin-4 and interleukin-13 signalling, key drivers
43 f three signaling complexes of the cytokines interleukin-4 and interleukin-13 with their receptors, s
44 fully human monoclonal antibody that blocks interleukin-4 and interleukin-13, has shown efficacy in
45 T lymphocytes (CTLs) and down-regulation of interleukin-4 and transforming growth factor- beta , lea
46 CD300a expression on memory B cells, whereas interleukin-4 and transforming growth factor-beta1 act a
47 ositive microglia, increased brain levels of interleukins 4 and 10, and reduced levels of CD68, F4/80
48 Local treatment, targeted at inhibition of interleukins 4 and 13 in the lung, could substantially d
49 her levels of Th-1 (interferon-gamma), Th-2 (interleukin-4), and Th-17 (interleukin-17)-associated cy
52 activator interferon gamma, the M2 activator interleukin 4, and M2-associated anti-inflammatory inter
53 nditions blocked up-regulation of GATA-3 and interleukin-4, and in effector/memory CD4(+) T cells, de
54 locyte-macrophage colony-stimulating factor, interleukin-4, and tumor necrosis factor-alpha and fused
55 evels of transforming growth factor beta and interleukin 4; and fewer myofibroblast infiltration (den
60 Exposure of peripheral blood monocytes to interleukin-4 can recapitulate the fusion process in vit
61 locyte-macrophage colony-stimulating factor, interleukin-4, CD40L, and interferon-gamma, resulting in
62 ith subsequent assay of interferon-gamma and interleukin 4 cell expression using ELISPOT technique.
64 ization status in C. neoformans-infected WT, interleukin-4-deficient (IL-4(-/-)), and gamma interfero
67 tor-dependent T helper 2 pathway that guides interleukin-4-dependent macrophage polarization, which i
68 chemical inhibition of PARP activity blocked interleukin-4-dependent transcription from target promot
69 pient invariant natural killer T-cell (iNKT) interleukin-4-driven expansion of donor Foxp3(+) natural
70 , in protein ubiquitination, and in insulin, interleukin-4, epidermal growth factor, and platelet-der
71 fibroblasts] responds to stimuli (bleomycin, interleukin-4, etc) with increased latent transforming g
72 exposed to Hb:haptoglobin complexes, but not interleukin-4, expressed the M(Hb) phenotype and were ch
73 early slowly progressing stages, augmenting interleukin-4 expression and protective M2 microglia, an
74 ay be mediated by the augmented secretion of interleukin-4 from mutant Cu2+/Zn2+ superoxide dismutase
75 r levels of mRNAs for PD-1, CD4, CD8, F4/80, interleukin-4, gamma interferon, granzyme A, and granzym
81 2,6-sialylated glycoform of IgG Fc to induce Interleukin 4 (IL-4) and Signal Transducer and Activator
84 ansforming growth factor-beta (TGF-beta) and interleukin 4 (IL-4) control the differentiation of CD4(
87 g cytokines interferon gamma (IFN-gamma) and interleukin 4 (IL-4) in the regulation of mycoplasma-spe
90 ected deer mice, including activation of the interleukin 4 (IL-4) pathway in T cells and B cells.
92 ic deficiency in KLF2 but instead was due to interleukin 4 (IL-4) produced by an expanded population
94 e show that interferon-gamma (IFN-gamma) and interleukin 4 (IL-4) signaled to the majority of lymphoc
96 eukin 4 receptor alpha (IL-4Ralpha)(-/-) and interleukin 4 (IL-4)(-/-) BALB/c mice have indicated tha
98 lon and Igamma1 transcription in response to interleukin 4 (IL-4), hence class switching to IgE and I
99 tact-sensitized mice preferentially produced interleukin 4 (IL-4), IL-10, and IL-17; CD8(+) T cells,
102 tein CIS, which was substantially induced by interleukin 4 (IL-4), negatively regulated the activatio
103 become lodged in the host liver, evoking an interleukin 4 (IL-4)- and IL-13-mediated dominant CD4(+)
104 is required for the phenotypic conversion of interleukin 4 (IL-4)-activated monocyte-derived F4/80(in
106 xpression and terminally differentiated into interleukin 4 (IL-4)-producing NKT2 cells or IL-17-produ
107 XCL13 were also necessary for development of interleukin 4 (IL-4)-producing type 2 helper T cells (T(
109 ease in the median fluorescence intensity of interleukin 4 (IL-4; P < .05) and interleukin 10 (IL-10;
110 iven via the alpha-chain of the receptor for interleukin 4 (IL-4Ralpha) is important for immunity to
111 ction/luciferase reporter assays, heightened interleukin-4 (IL-4) -induced activation of target genes
112 n monocytes were differentiated into iDCs by interleukin-4 (IL-4) and granulocyte-macrophage colony-s
113 infected BALB/c-CXCR3(Tg) mice produced more interleukin-4 (IL-4) and IL-10 and less gamma interferon
115 by which the T helper 2 (Th2) cell cytokines interleukin-4 (IL-4) and IL-13 mediate their effects on
117 ifferent class of proinflammatory cytokines, interleukin-4 (IL-4) and IL-13, in the induction of infl
119 aracterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcrip
120 l BEAS-2B cells by proinflammatory cytokines interleukin-4 (IL-4) and tumor necrosis factor alpha (TN
121 the control of the archetypal T(H)2 cytokine interleukin-4 (IL-4) and was a fundamental component of
124 e combination therapy of gemcitabine with an interleukin-4 (IL-4) cytotoxin composed of IL-4 and trun
127 hown that the type 2 cell signature cytokine interleukin-4 (IL-4) hampers neutrophil expansion and mi
129 ere we show an increase in the production of interleukin-4 (IL-4) in p38alpha(-/-) CD4(+) T cells in
131 cells (Tfh cells) are the major producers of interleukin-4 (IL-4) in secondary lymphoid organs where
135 that inhibition of Th2 differentiation using interleukin-4 (IL-4) or IL-13 blockade prevents initiati
136 crophage markers by a mechanism dependent on interleukin-4 (IL-4) or interleukin-13 (IL-13) activatio
139 ation in Socs2(-/-) macrophages and enhanced interleukin-4 (IL-4) plus IL-13-induced STAT6 phosphoryl
140 der exposure to S. haematobium eggs triggers interleukin-4 (IL-4) production and makes BALB/c mice su
142 TMEV-specific lymphoproliferative responses, interleukin-4 (IL-4) production, and IL-4/gamma interfer
143 as partially mediated by CD4+ T cells and by interleukin-4 (IL-4) production, did not require eosinop
144 was associated with exposure, with increased interleukin-4 (IL-4) production, IL-5 transcription, and
145 n (TSLP) and type 2 immunity, in particular, interleukin-4 (IL-4) production, in mediating hepatic eo
147 ith the ability of IRF4/PU.1 to activate the interleukin-4 (IL-4) promoter, strongly suggesting a rol
148 -gamma) recall responses rather than reduced interleukin-4 (IL-4) responses, suggesting that immunopa
150 mbinant RSV vectors expressing IFN-gamma and interleukin-4 (IL-4) that allow us to explore the role o
151 ha (TNF-alpha), lipopolysaccharide (LPS), or interleukin-4 (IL-4) to induce classic (M1 and M(LPS)) o
153 rates in mice deficient in the Th2 cytokine interleukin-4 (IL-4) via STAT6 mutation in a BALB/c back
157 n NKT-cell-deficient Jalpha18(-/-) hosts and interleukin-4 (IL-4)(-/-) hosts, or when the donor trans
158 thal ischemia, local neurons rapidly produce interleukin-4 (IL-4), a cytokine with potent anti-inflam
159 reduced levels of ileal transcripts encoding interleukin-4 (IL-4), a key mediator of intestinal masto
160 marked reductions in cysteinyl leukotrienes, interleukin-4 (IL-4), and IL-10, and both ATLa and ZK-99
162 feron were also up-regulated, while eotaxin, interleukin-4 (IL-4), and IL-5 were down-regulated.
163 r expansion is driven by the type 2 cytokine interleukin-4 (IL-4), as well as by M-CSF, which also co
164 S mice exposed to mercury, the production of interleukin-4 (IL-4), but not that of IL-2 or interferon
167 ited increased production of CD4(+)-specific interleukin-4 (IL-4), IL-5, and IL-13 and CD4(+)Foxp3(+)
168 s of type II immunity, such as production of interleukin-4 (IL-4), IL-5, and IL-13 by whole-lung cell
169 produce a wide range of cytokines, including interleukin-4 (IL-4), IL-5, IL-13, interferon-gamma, IL-
170 Type 2 inflammatory cytokines, including interleukin-4 (IL-4), IL-5, IL-9, and IL-13, drive the c
171 -type and Th2-promoting cytokines, including interleukin-4 (IL-4), IL-5, IL-9, IL-13, IL-31, and thym
172 as an anti-TIM-3 polyclonal Ab, can promote interleukin-4 (IL-4), IL-6, and IL-13 production without
173 pstream stimuli of these pathways, including interleukin-4 (IL-4), IL-6, and IL-13, increased dramati
174 cells was inhibited by even small amounts of interleukin-4 (IL-4), IL-6, and interferon-gamma (IFN-ga
175 onators, the cytokines interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-5 (IL-5), and tumor ne
176 repair is a subset of a broad repertoire of interleukin-4 (IL-4)- and IL-13-dependent host responses
177 opment but instead promoted the formation of interleukin-4 (IL-4)-committed T follicular helper (Tfh)
178 e lung, surfactant protein A (SP-A) enhanced interleukin-4 (IL-4)-dependent macrophage proliferation
182 ly (P </= 0.001) decreased the percentage of interleukin-4 (IL-4)-positive CD4 and CD8 cells in RSV-s
183 ort, we demonstrate that KSHV suppresses the interleukin-4 (IL-4)-stimulated immune response of B-lym
184 rt in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative m
194 ulatory/anti-inflammatory cytokine response (interleukin-4 [IL-4] plus IL-10 > tumor necrosis factor
195 e Th1 (gamma interferon [IFN-gamma]) or Th2 (interleukin-4 [IL-4]) cytokines, with detailed monitorin
196 tors known to generate either alternatively (interleukin-4 [IL-4]) or classically (macrophage colony-
197 ll functions by anti-inflammatory cytokines (interleukin-4 [IL-4], IL-10, and transforming growth fac
198 tes/macrophages, or the levels of cytokines (interleukin-4 [IL-4], IL-10, gamma interferon, or IL-13)
199 y inflammatory cell influx and Th2 cytokine (interleukin-4 [IL-4], IL-5, and IL-13) content relative
207 Mo-MLV insertion region 1 homolog (BMI1) and interleukin-4 (IL4) expression, resulting in decreased G
208 The four cytokines erythropoietin (EPO), interleukin-4 (IL4), human growth hormone (hGH), and pro
212 showed that CD4(+) T cells were a source of interleukin-4 in infected CCR2(-/-) mice, but their cont
213 the data indicate that generation of excess interleukin-4 in lungs of H. capsulatum-infected CCR2(-/
215 phage-colony-stimulating factor (GM-CSF) and interleukin-4 induce monocyte differentiation into moDCs
216 Moreover, AR activation upregulated the interleukin-4-induced expression of CCAAT/enhancer-bindi
217 d a positive effect on interferon-gamma- and interleukin-4-induced JAK/STAT activity in HEK293 or HEK
218 Stimulation of B cells with anti-CD40 plus interleukin-4 induces CSR from Cmu to Cgamma1 (IgG1) and
221 alpha) and downregulation of Th2 cytokines (interleukin 4, interleukin 5, interleukin 10, interleuki
222 cytokine production showed higher levels of interleukin-4, interleukin-12, and eotaxin mRNA expressi
223 both in vitro and in vivo, with more robust interleukin-4, interleukin-5, and interleukin-13 product
224 Plasma was assayed for interleukin-1beta, interleukin-4, interleukin-5, interleukin-6, interleukin
225 Level of interleukin-1beta, interleukin-2, interleukin-4, interleukin-5, interleukin-6, interleukin
226 1beta, soluble interleukin-2 receptor-alpha, interleukin-4, interleukin-5, interleukin-7, interleukin
228 d significant differences between groups for interleukin-4, interleukin-6, interleukin-9, interleukin
231 ts of wild-type and cytokine gene-deficient (interleukin-4-knockout [IL-4 (-/-)] and interferon-gamma
235 stantially more immunotherapeutic sustaining interleukin-4 levels and M2 microglia, and resulting in
239 A expression of the T-helper type 2 cytokine interleukin-4 (P = 0.001) than animals without schistoso
240 T cells (P=0.01), and reduced expression of interleukin-4 (P=0.02) in gal-3 null mice suggest possib
243 ietic cell transplantation demonstrated that interleukin-4 polarized human T-Rapa cells had a mixed T
244 that nonpolarized (M0) as well as M1 or M2 (interleukin-4) polarized IPSDM shared transcriptomic pro
249 tigen-specific CD4+ T cell proliferation and interleukin 4 production in vitro, and transfer of basop
250 s following the enhancement of virus-induced interleukin-4 production and subsequent DC-SIGN expressi
251 lso suppressed IFN-gamma and, in many cases, interleukin-4 production by CD4+ T cells at concentratio
252 ction, CD301b(+) DC depletion led to blunted interleukin-4 production by OVA-specific OT-II transgeni
253 n delta-toxin, promoted immunoglobulin-E and interleukin-4 production, as well as inflammatory skin d
255 Stimulation of B cells with CD40 ligand and interleukin-4 promoted their ability to transinfect hepa
257 n gamma (IFN-gamma) receptor (IFN-gammaR) or interleukin 4 receptor alpha (IL-4Ralpha) were infected
259 Focal demyelination in mice lacking IL4I1 or interleukin 4 receptor alpha (IL4Ralpha) results in incr
260 susceptible (Il4ra(F709)) mice with enhanced interleukin-4 receptor (IL-4R) signaling exhibited STAT6
261 s long been established that dimerization of Interleukin-4 receptor (IL-4R) subunits is a pivotal ste
262 ulation of interleukin-1 receptor 1 (IL1r1), interleukin-4 receptor (IL4r), fibroblast growth factor
263 reg) cells in a manner that was dependent on interleukin-4 receptor alpha (IL-4Ralpha) expression in
264 ion, and we demonstrated a role for enhanced interleukin-4 receptor alpha (IL-4Ralpha) expression on
265 monstrated that, during skin repair in mice, interleukin-4 receptor alpha (IL-4Ralpha)-dependent macr
269 oclonal antibody to the alpha subunit of the interleukin-4 receptor, in patients with persistent, mod
270 inants governing the assembly of the type II interleukin-4 receptor, taking advantage of various agon
272 ergy expenditure in wild-type, Ucp1(-/-) and interleukin-4 receptor-alpha double-negative (Il4ra(-/-)
273 involved in PH etiology, PH still occurs in interleukin-4 receptor-deficient mice under these condit
278 -induced ATM infiltration and potentiator of interleukin-4 responses and point toward a crucial role
280 regulating t-bet gene expression, decreasing interleukin 4 secretion, and downregulating gata3 gene e
284 in human CLL was induced by stimulation with interleukin 4/soluble CD40 ligand and by stroma cell con
285 gamma interferon and interleukin-12, but no interleukin-4, suggesting an induction of a T helper 1 r
286 Using IgG as a model cross-reactant with the interleukin-4 system, we additionally illustrate techniq
287 st cells may have resulted in a low level of interleukin-4 that contributed to the reduction in the m
290 erived dendritic cell-mediated regulation of interleukin-4 transcription was dependent on major histo
294 tively activated" M2 macrophages obtained by interleukin 4 treatment, but almost missing in M1 macrop
296 ess the therapeutic effect of pitrakinra, an interleukin-4 variant that targets allergic Th2 inflamma
297 kine, GIFT4, engineered by fusing GM-CSF and interleukin-4, was previously found to simulate B cell p
299 tic cells produced interferon gamma, but not interleukin 4, when stimulated with nonstructural 5.
300 g CTLA4-Ig therapy had lower serum levels of interleukin 4, whereas mice receiving anti-TNF therapy h
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